Magnetic Particle-Based Hybrid Platforms for Bioanalytical Sensors

Biomagnetic nano and microparticles platforms have attracted considerable interest in the field of biological sensors due to their interesting physico-chemical properties, high specific surface area, good mechanical stability and opportunities for generating magneto-switchable devices. This review discusses recent advances in the development and characterization of active biomagnetic nanoassemblies, their interaction with biological molecules and their use in bioanalytical sensors

I-R rats

I-R rats - hdcv data file

Control rats

Control rats - hdcv data file

Early changes in transient adenosine during cerebral ischemia and reperfusion injury.

Adenosine is an important neuromodulator in the central nervous system, and tissue adenosine levels increase during ischemic events, attenuating excitotoxic neuronal injury. Recently, our lab developed an electrochemical fast-scan cyclic voltammetry (FSCV) method that identified rapid, spontaneous changes in adenosine concentrations that last only about 3 seconds. Here, we investigated the effects of cerebral ischemia and reperfusion on the concentration and frequency of transient adenosine release in the caudate-putamen. In anesthetized rats, data were collected for four hours: two hours of normoxia, 30 min of cerebral ischemia induced by bilateral common carotid artery occlusion, and 90 min of reperfusion. Transient adenosine release was increased during the cerebral ischemia period and remained elevated during reperfusion. The total number of adenosine transients increased by 52% during cerebral ischemia and reperfusion compared to normoxia. The concentration of adenosine per event did not increase but the cumulative adenosine concentration during cerebral ischemia and reperfusion increased by 53% because of the higher frequency of events. Further, we evaluated the role of A2A antagonist, SCH442416, a putative neuroprotective agent to affect adenosine transients. SCH442416 significantly decreased the transient frequency during cerebral ischemia-reperfusion by 27% and the cumulative concentration by 31%. Our results demonstrate that this mode of rapid adenosine release increases during early cerebral ischemia-reperfusion injury. Rapid adenosine release could provide fast, local neuromodulation and neuroprotection during cerebral ischemia

A2A rats

A2A-stroke rats - hdcv data file

Data from: Early changes in transient adenosine during cerebral ischemia and reperfusion injury

Adenosine is an important neuromodulator in the central nervous system, and tissue adenosine levels increase during ischemic events, attenuating excitotoxic neuronal injury. Recently, our lab developed an electrochemical fast-scan cyclic voltammetry (FSCV) method that identified rapid, spontaneous changes in adenosine concentrations that last only about 3 seconds. Here, we investigated the effects of cerebral ischemia and reperfusion on the concentration and frequency of transient adenosine release in the caudate-putamen. In anesthetized rats, data were collected for four hours: two hours of normoxia, 30 min of cerebral ischemia induced by bilateral common carotid artery occlusion, and 90 min of reperfusion. Transient adenosine release was increased during the cerebral ischemia period and remained elevated during reperfusion. The total number of adenosine transients increased by 52% during cerebral ischemia and reperfusion compared to normoxia. The concentration of adenosine per event did not increase but the cumulative adenosine concentration during cerebral ischemia and reperfusion increased by 53% because of the higher frequency of events. Further, we evaluated the role of A2A antagonist, SCH442416, a putative neuroprotective agent to affect adenosine transients. SCH442416 significantly decreased the transient frequency during cerebral ischemia-reperfusion by 27% and the cumulative concentration by 31%. Our results demonstrate that this mode of rapid adenosine release increases during early cerebral ischemia-reperfusion injury. Rapid adenosine release could provide fast, local neuromodulation and neuroprotection during cerebral ischemia

Stereoselective synthesis of syn-&#946;-amino esters using the TiCl<SUB>4</SUB>/R<SUB>3</SUB>N reagent system

The reactions of benzaldehyde imines and esters with the TiCl4/R3N reagent system give syn-&#946;-amino esters as the major products in 38–87% yields

Effect of the A_2A antagonist, SCH442416 (3 mg/kg. i.p), on adenosine on adenosine transients during stroke.

<p>All data and statistics are for n = 8 animals. (A) Number of adenosine transients decreased significantly after SCH442416 during stroke (paired t-test, p = 0.01). (B) Inter-event time of all adenosine transients. The exponential fit (black line) during normoxia (predrug) is y = 0.5981e^-0.0207x (R² = 0.99) and SCH442416 + ischemia-reperfusion (red line) is y = 0.4491e^-0.0155x (R² = 0.99). After SCH442416 treatment, the inter-event time was significantly longer during stroke, with a median inter-event time change from 39 s (normoxia) to 48 s (I-R). There was a significant difference between the distributions before and after stroke (KS-test, p = p < 0.0001). (C) The average event adenosine concentration per transient after SCH442416 administration during ischemia and reperfusion 0.13 ± 0.01 μM (n = 759 transients) compared to normoxia 0.14 ± 0.01 μM (n = 1030 transients) was not significantly different (unpaired t-test, n = 8 animals, p = 0.05) (D) There was no significant change in the median cumulative concentration after SCH442416 during stroke compared to normoxia (p = 0.11).</p

Control experiments with no ischemia.

<p>All data and statistics are for n = 7 animals (A) Number of adenosine transients did not change between the 1^st and 2^nd 2 hour periods (paired t-test, p = 0.48). (B) Inter-event time of all adenosine transients. The exponential fit (black line) in the first 2 h is y = 0.5592e^-0.0207x (R² = 0.99) and in the second 2 h (grey line) is y = 0.5195e^-0.0172x (R² = 0.99). There was no significant difference between the underlying distributions in the first 2 h and second 2 h (KS-test, n = 7 animals, p = 0.6). (C) The average event adenosine concentration per transient. There was no significant change in the average adenosine concentration per transient for first 2 hrs (n = 1084) and second 2 hrs (n = 1064) (unpaired t-test, n = 7 animals, p = 0.12). (D) There was no significant change in the mean cumulative concentration between the 1^st and 2^nd 2 hour periods (paired t-test, p = 0.55).</p

Spontaneous adenosine release frequency and concentration in the caudate-putamen during stroke.

<p>All data and statistics are for n = 10 animals. (A) The average event adenosine concentration per transient for normoxia (n = 829) and ischemia-reperfusion (n = 1306) was not significantly different (unpaired t-test, n = 10 animals, p = 0.57) (B) Average event adenosine concentration per transient were divided into 30 min periods during normoxia, ischemia and reperfusion periods and event concentration did not show any significant difference (One-way ANOVA, p = 0.9354) (C) The cumulative adenosine concentration was significantly different after stroke compared to normoxia (paired t-test, n = 10 animals, p = 0.03). (D) Cumulative adenosine concentration was divided into 30 min periods. The first four bars are 30 min periods during normoxia, then one bar for the 30 min of ischemia, followed by three 30 min bars for the total 90 min of reperfusion. The dashed lines show the average for the normoxia and ischemia-reperfusion periods. Cumulative concentration during normoxia, ischemia and reperfusion was significantly different (One-way ANOVA, p = 0.0022).</p