Recommended methods for cytological procedures in haematology. International Committee for Standardization in Haematology (ICSH).
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Biomedical subjects
Publications and source records attributed to A Shibata.
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The effect of neuropeptide Y (NPY) on the coronary circulation of the closed-chest dogs (n = 7) was studied. The left circumflex artery was cannulated and perfused with arterial blood withdrawn from the femoral artery. The flow was kept constant by a roller pump and it was monitored by an electromagnetic flowmeter. An increase in the perfusion pressure which was characterized by a slow onset and long-lasting effect (more than 10 min) was found in each dog after NPY. There were no significant changes in the arterial blood pressure, central venous pressure and heart rate. The peak rise was observed at about 1 min; from 108 +/- 9 mmHg to 144 +/- 13 mmHg (mean +/- SE) (p less than 0.01). This increase in the perfusion pressure resulted from vasoconstriction distal to the cannula. When the doses of NPY was changed, a dose-response relation was found (n = 4). Phentolamine did not inhibit the vasoconstrictor effect of NPY (n = 4). The endogeneous substance NPY might be engaged in the regulation of myocardial perfusion and can be a candidate responsible for coronary spasm.
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In order to clarify the intracellular localization of salivary peptide P-C-like immunoreactivity in human pancreatic B-cells, an immunohistochemical study at electron microscopic levels was carried out by the protein A-gold technique using antisera against insulin and salivary peptide P-C. Both salivary peptide P-C-like immunoreactivity and insulin-like immunoreactivity were present only in the insulin secretory granules of the pancreatic B-cells. However, the former immunoreactivity was lacking in many insulin secretory granules of foetal pancreatic B-cells while the latter immunoreactivity was seen in all insulin secretory granules. Salivary peptide P-C-like immunoreactivity was not found in the other kinds of cells in the islets. In a previous immunohistochemical study at light microscopic level, salivary peptide P-C-like immunoreactivity appeared in a few pancreatic B-cells at about the 16th week of gestation, in an increasing number during gestation, and was seen in all pancreatic B-cells a few months after birth. The present finding together with the above results suggest that absence of salivary peptide P-C-like immunoreactivity in some foetal pancreatic B-cells may be due to the underdevelopment of salivary peptide P-C-like immunoreactivity in each insulin secretory granule. From the examination of cross-reactivity of antisera against salivary peptide P-C to other kinds of salivary peptides and salivary Protein C, and from the results of an indirect immunofluorescence technique using three kinds of antisera including antisera against salivary peptide P-C, salivary peptide P-B and salivary Protein C, it was thought that salivary peptide P-C-like immunoreactivity in human pancreatic B-cells belongs neither to salivary Protein C nor to salivary peptide P-B nor to salivary peptide P-E, but either to salivary peptide P-C itself or to an unknown substance which has common antigenic determinants with salivary peptide P-C, salivary peptide P-B and salivary Protein C. Salivary peptide P-C-like immunoreactivity was not found in the pancreatic B-cells of other mammals. Thus, although a new substance other than insulin is present in the insulin secretory granules of the human pancreatic B-cells, its pathophysiological function remains unclear.
An indirect immunofluorescence technique using antisera against salivary peptide P-C and against salivary Protein C was carried out on the laryngeal, tracheal and bronchial glands to examine whether salivary peptide P-C-like immunoreactivity, recently demonstrated in the serous cells of the human salivary glands, was also present in those of laryngeal, tracheal and bronchial glands and to ascertain whether salivary peptide P-C is a fragment of salivary Protein C or not. Salivary peptide P-C-like immunoreactivity was present in the serous cells of the human laryngeal, tracheal and bronchial glands. Observation of serial sections immunostained with two kinds of antisera revealed that cells reacting with antisera against salivary peptide P-C were identical to those reacting with antisera against salivary Protein C pre-incubated with salivary peptide P-C. The finding implied that salivary peptide P-C and salivary Protein C, originally isolated from human saliva, were also present in the serous cells of tissues other than the salivary glands. Furthermore, analysis of the primary structure of salivary peptide P-C and salivary Protein C together with the present morphological finding suggests that salivary peptide P-C is a COOH-terminal fragment of salivary Protein C. Thus, salivary Protein C and salivary peptide P-C may play some role in the function of the serous cells of the salivary and laryngo-tracheo-bronchial glands.
Analysis of beat to beat changes in left ventricular (LV) ejection time during cardiac pacing was utilized to assess the atrial contribution to ventricular filling in 30 consecutive patients undergoing diagnostic cardiac catheterization. The group consisted of 9 normal subjects, 18 with coronary artery disease and 3 with congestive cardiomyopathy. The recordings of aortic pressure were made during atrial pacing and ventricular pacing at a rate 5 to 10 beats/min above each individual's sinus rhythm. During ventricular pacing, LV ejection time was the longest when an atrial contraction preceded a ventricularly paced beat by a physiologic interval and was approximately similar to that obtained during atrial pacing (maxET). When the atrial systole occurred with or followed the ventricularly paced contraction, LV ejection time was decreased (minET). Since maxET occurred in the presence of an effective atrial contraction to ventricular filling and minET in the absence of this contraction, the atrial contribution to ventricular filling was calculated as (maxET-minET)/maxET X 100 (%). LV volumes at end-systole (V1), before atrial contraction (V2) and at end-diastole (V3) were obtained according to the area-length method by tracing the silhouette of left ventriculograms using a computer system. The atrial contribution was calculated from LV volumes using the formula (V3-V2)/(V3-V1) X 100 (%). There was a good correlation (r = 0.88) between the atrial contributions calculated from LV ejection times and those calculated from LV volumes. In the patients with coronary artery disease and with congestive cardiomyopathy, the atrial contribution was significantly greater than in the normal subjects. The measurement of LV ejection time during ventricular pacing may be a clinically useful screening procedure to identify patients in whom physiologic pacing may be indicated.
Twenty-six patients with idiopathic dilated cardiomyopathy (DCM) underwent thallium-201 myocardial scintigraphy. Nine patients (group A) showed a perfusion defect in the interventricular septum (IVS) and 7 patients (group B) showed a defect in the left ventricular posterior wall (LVPW). Hemodynamic responses and catecholamine levels were compared between 16 patients (DCM group) and 6 control subjects (control group) following dopamine infusion (6 micrograms/Kg/min). The end-diastolic thickness of the IVS and LVPW, and the percentage wall thickening were assessed by echocardiography. Plasma dopamine and norepinephrine concentrations in the DCM group were not different from those of the control group at rest. During the dopamine infusion, however, norepinephrine increased only in the control group. There were significant differences in the thickness of the IVS among the 3 groups [7.3 +/- 1.4 mm for group A (p less than 0.001 vs control and p less than 0.05 vs group B), 8.9 +/- 1.5 mm for group B (p less than 0.01 vs control), 10.2 +/- 1.5 mm for the control group]. The percentage thickening of the IVS increased during the dopamine infusion in group B only and the thickening of the LVPW increased in group A only. Thus, in the myocardium of DCM patients with thallium perfusion defects, the degree of thickening did not change during dopamine infusion, but in the myocardium of DCM patients with normal thallium uptake the percentage thickening increased more than in the control group.
Two young males who had no organic heart disease died unexpectedly during the night. In one patient, the monitor ECG showed a sinoatrial block and the electrophysiologic study revealed a sinoatrial conduction time at the upper limit of normal and a prolonged PA interval. The surface ECG showed left axis deviation. Ventricular ectopic beats were confined to the night when he died from ventricular flutter. The ECG of the other patient was normal except for the change in QRS configuration found when the preceding RR interval was prolonged, suggesting a phase 4 block in intraventricular conduction. He was completely free from arrhythmia except for the ventricular ectopic beats which developed around 9:00 p.m. and the ventricular flutter following an R-on-T type ventricular ectopic beat which resulted in death during the night. The autopsy showed no organic heart disease. ST elevation suggestive of acute ischemia was not found and the QT intervals were normal in both cases. No electrolyte imbalances were found. These 2 cases can be diagnosed as pokkuri disease which is well known in Japan. The victims are exclusively young males who have no apparent diseases to which death can be attributed.
We report on a 15 year old patient with Duchenne's progressive muscular dystrophy who demonstrated a narrowing of the left ventricular inflow and outflow tracts due to compression by a highly deformed thoracic spine. A systolic murmur (4/6) with thrill and a diastolic murmur (2/6) were heard, with these murmurs being louder in the expiratory phase as compared with the inspiratory phase. The second heart sound showed a paradoxical splitting. Echocardiograms revealed a compressed and narrowed left ventricle and a prolapsed mitral valve. The intensities of the heart murmurs changed synchronously with the chamber's narrowing due to respiration. A narrowed left ventricle occurring as a result of the compression by the deformed thoracic spine is thought to be the cause of these cardiac findings.
In nine patients with chronically implanted ventricular pacemaker (VVI), diurnal variation of the QT interval was studied. The mean age of the patients was 74.2 years and underlying diseases were atrioventricular block (three patients), sick sinus syndrome (four patients) and chronic atrial fibrillation with bradycardia and heart failure (two patients). Eight of the nine patients showed longer QT intervals during sleep than during waking. Only one patient showed no change in QT interval during sleep and during wake time. The mean QT interval of the nine patients at each hour was slightly longer (9 msec) during sleep than that during each awake hour (p less than 0.001). The prolongation of QT interval during sleep may offer a possible mechanism of some nocturnal arrhythmias.
Atrioventricular (AV) block was produced in animals for experimental purposes by use of a newly devised cannula. It has bipolar electrodes; one electrode on the needle tip and the other 5.0 mm proximally from the tip. Otherwise, the cannula was electrically completely insulated. The cannula was inserted from the right external jugular vein and advanced close to the AV ring. While His bundle electrogram was obtained with the electrodes, the AV node was accessed. The injection site was determined as the point where His bundle electrogram can be well recorded and the atrial electrogram is close to or larger than the ventricular electrogram in amplitude. Xylocain solution, 0.2 to 0.4 ml, was injected with the syringe attached on the other end of the cannula. Transient AV block occurred when the needle tip was properly positioned. Then, 0.2 ml to 0.4 ml of anhydrous alcohol was added to make permanent a AV block. A possible application of this technique was implicated.
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