High-frequency repetitive transcranial magnetic stimulation improves refractory depression by influencing catecholamine and brain-derived neurotrophic factors.

INTRODUCTION: Repetitive transcranial magnetic stimulation (rTMS) is a non-invasive and easily tolerated method of altering cortical physiology. To date, numerous open and sham controlled clinical trials have explored the antidepressant potential of rTMS. In the present study, we investigated clinical trials of high-frequency rTMS (20 Hz) for treatment of refractory depression, and also examined the effect of rTMS on plasma levels of catecholamine metabolites and brain-derived neurotropic factor (BDNF). METHODS: Twenty-six depressed inpatients who met the DSM-IV criteria for major depressive disorder and had failed to respond to treatment with at least two antidepressant drugs given at adequate doses (above 150 mg/day in an equivalent dose of imipramine) and durations (at least 4 weeks for each drug) were enrolled in this study. Eleven were males, 15 females. The ages of the subjects ranged from 19 to 78 years old (mean +/- SD = 52.9 +/- 17.8). All patients were administered left prefrontal 20 Hz rTMS at 80 % MT (total 800 pulses a day) over ten daily sessions. The plasma levels of 3-methoxy-4-hydroxyphenylglycol (MHPG) and homovanillic acid (HVA) were analyzed by high-performance liquid chromatography. The plasma levels of BDNF were also measured with the sandwich ELISA method. RESULTS: The mean 17-item Hamilton Rating Scale for Depression (Ham-D) score of 20.5 +/- 5.2 before rTMS was significantly decreased to 15.6 +/- 7.3 after rTMS. Nine of 26 patients (35 %) demonstrated some improvement (Ham-D > or = 25 %) by rTMS. The levels of plasma MHPG, but not those of HVA, were significantly reduced after rTMS treatment, and a negative correlation was observed between the change in plasma MHPG levels and the change in scores of agitation. In addition, the plasma levels of BDNF were significantly increased by 23 % in responders and partial responders, but not in nonresponders, after rTMS treatment, and a trend for association was found between the changes in Ham-D scores and changes in plasma BDNF levels in all patients after rTMS treatment. CONCLUSION: These results suggest that rTMS treatment brings about some improvement in refractory depression, especially for symptoms such as agitation, by influencing MHPG and BDNF, which is in accordance with previous reports showing that BDNF was increased by various antidepressants treatments.

New antibody immobilization method via functional liposome layer for specific protein assays.

A specific protein assay system based on functional liposome-modified gold electrodes has been demonstrated. To fabricate such assay system, a liposome layer was initially grown on top of a gold layer. The liposome layer contained two kinds of functional molecules: biotin molecules for the binding sites of streptavidin and N-(10,12-pentacosadiynoic)-acetylferrocene molecules for the facile redox probe in electrochemical detections. Then, streptavidin was attached on the functional liposme-modified layer using the interaction of streptavidin-sbiotin complex. On the streptavidin-attached surface, antibody molecules, anti-human serum albumin antibodies could be immobilized without any secondary antibodies. AFM imaging of the streptavidin-attached liposome surface revealed a uniform distribution of closely packed streptavidin molecules. In situ quartz-crystal microbalance and electrochemical measurements demonstrated that the wanted antibody-antigen reactions should occur with high specificity and selectivity. Our specific antibody assay system, based on a functional liposome modified electrode, can be developed further to yield sophisticated structures for numerous protein chips and immunoassay sensors.

[Infarct size determined by emission computed tomography using 99mTc-PYP: effect of coronary thrombolysis].

Emission computed tomography with 99mTc-PYP was used to estimate infarct size in 38 patients with documented acute myocardial infarction. In the present study, the effect of thrombolysis with Urokinase on infarct size and on left ventricular function was assessed. Fourteen patients with acute myocardial infarction who underwent intracoronary thrombolysis within six hours after the onset of symptoms, and 24 patients who underwent conventional therapy were the subjects of this study. Infarct size was measured by drawing a region of interest around the myocardial pyrophosphate uptake for each tomographic slice. The boundary was then defined as 65% of the maximal count within the region of interest as determined by phantom volume studies. The total number of voxels was obtained by adding those in all slices and multiplying the sum by the voxel volume (0.205 ml per one voxel) to determine the infarct volume. Measurement of the 99mTc-PYP uptake on the tomographic image revealed an average infarct size of 100.1 +/- 36.0 ml (ranged 45 to 198). The calculated infarct volume correlated significantly with sigma CPK (p less than 0.01) and with left ventricular ejection fraction (p less than 0.01), but not with the peak CPK. In patients with acute inferior myocardial infarction, the mean infarct volume was 78.4 +/- 29.1 ml in the coronary thrombolysis group, and 105.1 +/- 33.7 ml in the conventional bypass graft treatment group (p less than 0.05). We concluded that successful intracoronary thrombolysis may reduce infarct size. ECT imaging with 99mTc-PYP to determine infarct size may be clinically applicable in patients with acute myocardial infarction.