[Scintigraphy presentation: Dual SPECT imaging of the myocardium with 201Tl and 99mTc].
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Biomedical subjects
Publications and source records attributed to K Nakai.
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To supplement catecholamine deficit in the brain with Parkinson disease, we have aimed to transplant the superior cervical ganglion (SCG), which contains norepinephrine and dopamine, into the brain. 1. Transplantation of SCG into rat cerebral cortex SCG was transplanted into the same rat's parietal cortex. Three weeks after the transplantation, catecholamine histofluorescence revealed many transplanted catecholamine cells in the cortex. However, no fibers extended from the transplanted tissue to the cerebral cortex. Some catecholamine fibers extended to the cerebral cortex where 6-OHDA (a specific neurotoxin to the catecholamine neuron) had been pretreated. 2. Transplantation of SCG into the caudate nucleus of MPTP-induced Parkinson monkey For animal model of Parkinson disease, MPTP (1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine) was administered to 5 monkeys. Tow weeks after MPTP administration, dopamine terminals disappeared in the caudate nucleus. After transplantation of SCG in the same animal, many transplanted SCG cells extended their axons to the caudate nucleus. The present results showed that transplanted SCG cells were well survived in the brain. Under a special circumstance such as shortage of catecholamine in the brain, transplanted SCG cells extended their axons into the brain. It is suggested that the transplantation of SCG can be a new therapy for Parkinson disease.
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Comparative evaluations of the percent of the perimetric circumference of infarction and cardiac performance for the occurrence of late potential were performed in 12 normal subjects and 22 patients with old myocardial infarction (MI). All patients were in normal sinus rhythm without bundle branch block. Bipolar X, Y, and Z leads were signal-averaged using a bandpass filter with a low-cut frequency of 100 Hz and a high-cut frequency of 300 Hz. The filtered signals for the three leads were displayed and combined into a vector magnitude, square root of X2 + Y2 + Z2. The percent ratio of the root mean square voltage in the last 40 msec of the QRS complex was calculated against that of the total filtered QRS (%RMS40). The value of the standard deviation (SD) in the phase distribution was obtained by the Fourier analysis of multi-gated blood pool images. Significant differences were observed among MI with late potential, MI without it and the normal subjects for %RMS 40 (5.7 +- 2.8% vs 26.9 +- 8.1, 37.5 +- 10.8%). Left ventricular ejection fraction was lower in MI with late potential (19.7 +- 7%) compared to that of MI without it (33 +- 18%) and the normal subjects (60 +- 4%); the value of SD was higher in MI with late potential (64 +- 21 degrees), compared to that of MI without it (43 +- 20 degrees) and the normal subjects (9 +- 4 degrees). These findings showed that the percent ratio of the last 40 msec RMS voltage (%RMS 40) was found to discriminate effectively among MI with and without late potential and normal subjects. It was suggested that the amount and structure of the infarcts may be important factors in the occurrence of late potential.
We developed the system of high-frequency analysis of the signal-averaged body surface ECG to detect low amplitude signals in the terminal portion of the QRS. Thirty-five patients four or more weeks after transmural myocardial infarction (MI) and 30 normal volunteers were studied. All patients were in normal sinus rhythm and did not have bundle branch block. Body surface ECG recording using bipolar X, Y, and Z leads was performed in a shielded room. One lead served as the reference. The three-channel amplifier was a commercially-available ECG system. The common mode rejection ratio was 120 dB. The signal from each lead was amplified and passed through an analogue filter (NF FV 624) with a low-cut frequency of 100 Hz and a high-cut frequency of 300 Hz. Then AD conversion was performed with 12-bit accuracy, 1024 samples/sec. The filtered signals for the three leads were displayed separately for each channel and were combined into a vector magnitude, square root of X2+Y2+Z2. The percent ratio of the root mean square voltage in the last 40 msec of the QRS complex to that of the total filtered QRS (%RMS40) and the duration of the filtered QRS were automatically calculated. These parameters obtained from the three groups were compared. Signal-averaged, non-filtered and filtered body surface ECGs were recorded using 25 (5 x 5 array) anterior chest unipolar leads in 20 normal volunteers and in patients with late potential. The departure index was calculated as the voltage differences between the mean value (M) in normal persons and the value in patients (Xi) with MI using the formula (Xi-M/SDi) at intervals every four msec. The departure maps, capable of identifying the location of the MI, were made from the departure index at four msec intervals; then the late potential (LP) area maps were superimposed on the departure maps. To determine the late potential, we used the filtered ECG of X, Y, and Z leads and quantitative values (%RMS 40) obtained from a vector magnitude incorporated in these three leads. Six MI patients, four anterior and two inferior, with the late potential had low amplitude signals at the end of the filtered QRS complex. The %RMS 40 was 6.8 +/- 2.9% (p less than 0.001) in MI patients with the late potential, 2.8 +/- 8.5% (p less than 0.01) in MI patients without the late potential, and 37 +/- 11% in normal subjects.(ABSTRACT TRUNCATED AT 400 WORDS)
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We studied biochemical and morphological changes in central catecholamine (CA) terminals in the kitten visual cortex following direct infusion with 4 mM 6-hydroxydopamine (6-OHDA) for a week. Two zones may be distinguished within the cortical area affected by 6-OHDA (a radius of approximately 10 mm). In the primary lesion zone (a radius of approximately 5 mm) near the center of the 6-OHDA infusion, excluding an area of non-specific damage left by cannulation (a radius of less than 1.5 mm), we found: (1) absence of fluorescent CA terminals by histochemistry; (2) very low desipramine-sensitive uptake of tritiated norepinephrine (NE) by cortical slices (desipramine-resistant NE uptake stayed high); (3) a 50% increase in beta-adrenoreceptor binding sites by densitometry of light microscopic autoradiograms; and (4) low levels (less than 20% of control) of endogenous NE and low to moderate levels (10-70%) of endogenous dopamine (DA). In the surrounding zone (about 5-10 mm from the infusion center), however, none of the above changes were observed, except for a moderate to substantial reduction (50-80% of control) in endogenous NE and a small (10-20%) reduction in endogenous DA. Within two weeks after the end of the cortical 6-OHDA infusion, the dimensions of the cortical area devoid of CA terminals became substantially smaller than those found earlier. Fluorescent CA terminals were seen virtually everywhere in the cortex by 4 weeks, including the scar left by placement of the infusion cannula. In 24 weeks CA terminals in the occipital cortex appeared close to normal in density as well as in fluorescence intensity. Biochemical assays also revealed the recovery trend of CA contents. A steady increase in the NE content was obtained in the surrounding zone, with the stronger trend at its periphery, eventually attaining full recovery in 23 weeks. The recovery was slow in the primary lesion zone, especially near the infusion center, though there was a continual increase in endogenous DA toward control even at the infusion center.
Ultrastructure of catecholaminergic (CA) terminals was studied in the kitten visual cortex which had been continuously infused with 6-hydroxydopamine (6-OHDA) for one week. Two methods were used to identify CA terminals: (1) cardiac perfusion with glyoxylic acid (GA) followed by potassium permanganate (KMnO4), a fixation method which leads to the precipitation of a dense core in CA-containing synaptic vesicles; and (2) induction by 6-OHDA of terminal degeneration in glutaraldehyde-fixed material. In material which was obtained from 3-week-survival animals and treated with GA-KMnO4, the 6-OHDA-infused hemisphere contained large terminal boutons (1-3 microns in diameter) having large dense-cored vesicles. Usual CA terminal boutons with small dense-cored vesicles were found only in the opposite control hemisphere. The unusual terminal boutons with large dense-cored vesicles were interpreted as "regenerative" CA terminals. They were no longer found in animals which survived for 33 weeks. Instead, the return of usual CA terminals filled with small dense-cored vesicles was noted. The above interpretation was further supported from the results of an additional two kittens in the 3-week group which received a single injection of 6-OHDA prior to their sacrifice (in addition to the initial 6-OHDA infusion 3 weeks before). In the glutaraldehyde-fixed sections, there were found terminal boutons filled with the accumulation of abnormal electron-dense material, suggesting the presence of ("regenerative") CA terminals in the 6-OHDA-infused cortex. The present results have thus provided further evidence for the presence of "regenerative" CA terminals in a cortical area in which CA terminals have been previously destroyed by cortical 6-OHDA infusion.
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The microangioarchitecture of corrosion casts of the cat spinal cord was studied by scanning electron microscopy. On the ventral surface of the spinal cord, the anterior spinal artery and the anterior spinal vein ran parallel along the anterior median fissure. Many central arteries branching from the anterior spinal artery coursed in a wavelike manner in the anterior median fissure. The number of central arteries was lowest in the thoracic spinal cord. Central arteries at some spinal cord levels revealed well-developed anastomoses with other central arteries in the anterior median fissure. These well-developed anastomotic central arteries were frequently observed in the thoracic spinal cord, in which the number of central arteries was lowest. On the dorsal surface of the spinal cord, the posterior spinal vein ran longitudinally at the midline and was drained by circumferential veins and posterior central veins. This vein formed a characteristic anastomotic plexus. Small arterioles (20 microns in diameter) in the spinal parenchyma revealed a ring-like compression at the branching site.
The role of intracortical vasoactive intestinal polypeptide (VIP)-containing neurons in the regulation of cortical blood flow was investigated in rats by immunohistochemical and hydrogen clearance methods. Immunohistochemical studies revealed an intimate association between intracortical VIP-containing neurons and small blood vessels. Intracortical injection of a VIP solution (10(-5) M) produced significantly higher blood flow in the treated cortex (mean +/- standard error of the mean: 46.2 +/- 4.0 ml/100 gm/min) than in the untreated cortex (36.9 +/- 2.4 ml/100 gm/min). These data suggest that intracortical VIP-containing neurons produce dilatation of intracortical blood vessels.
Transrectal longitudinal ultrasonography of the prostate was done for 20 patients with prostatic diseases, 12 with benign prostatic hypertrophy, 6 with bladder neck contracture, and 2 with chronic prostatitis. The intravesical protrusion of the prostate and the opening of the bladder neck, which can be easily recognized by this method, were discussed in relation to dysuria, using subjective symptoms, residual urine, and uroflowmetry (peak flow rate) as parameters. The former was slightly correlated to dysuria, and the latter was definitely correlated to dysuria.
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Human lymphoblastoid interferon (HLBI-alpha) or recombinant human leukocyte interferon (HLIF-alpha) was administered to ten patients suffering from renal cell carcinoma at a daily dose of 5 X 10(6) units. The efficacy of interferon was assessed in nine patients who had received HLBI-alpha or HLIF-alpha for more than eight weeks. One patient (11%) demonstrated complete response (CR), three patients (33%) showed no change and five patients (56%) continued to have progressive disease. CR was obtained after 30 weeks under HLBI-alpha and FT-207 combination therapy. The main side effects were fever, anorexia, general fatigue and hematologic toxicities. Cessation of interferon therapy due to side effects was necessary in three patients. In conclusion interferon is one of the most valuable agents in the treatment of renal cell carcinoma.
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