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Due to the structural similarity to N-methyl-4-phenyl pyridinium (MPP(+)), paraquat might induce dopaminergic toxicity in the brain. However, its blood--brain barrier (BBB) penetration has not been well documented. We studied the manner of BBB penetration and neural cell uptake of paraquat using a brain microdialysis technique with HPLC/UV detection in rats. After subcutaneous administration, paraquat appeared dose-dependently in the dialysate. In contrast, MPP(+) could not penetrate the BBB in either control or paraquat pre-treated rats. These data indicated that the penetration of paraquat into the brain would be mediated by a specific carrier process, not resulting from the destruction of BBB function by paraquat itself or a paraquat radical. To examine whether paraquat was carried across the BBB by a certain amino acid transporter, L-valine or L-lysine was pre-administered as a co-substrate. The pre-treatment of L-valine, which is a high affinity substrate for the neutral amino acid transporter, markedly reduced the BBB penetration of paraquat. When paraquat was administered to the striatum through a microdialysis probe, a significant amount of paraquat was detected in the striatal cells after a sequential 180-min washout with Ringer's solution. This uptake was significantly inhibited by a low Na(+) condition, but not by treatment with putrescine, a potent uptake inhibitor of paraquat into lung tissue. These findings indicated that paraquat is possibly taken up into the brain by the neutral amino acid transport system, then transported into striatal, possibly neuronal, cells in a Na(+)-dependent manner.

Previous studies reported the existence of both D1- and D2-like receptors in the cortical collecting duct (CCD). However, especially with regard to natriuresis, it remains controversial. In the present study, rabbit CCD was perfused to characterize the receptor subtypes responsible for the tubular actions. Basolateral dopamine (DA) induced a dose-dependent depolarization of transepithelial voltage. Basolateral domperidone, a D2-like receptor antagonist, abolished depolarization, whereas SKF-81297, a D1-like receptor agonist, showed no significant change. In addition, bromocriptine, a D2-like receptor agonist, also caused depolarization, whereas SKF-81297, a D1-like receptor agonist, did not depolarize significantly. Moreover, RBI-257, a D4-specific antagonist, reversed the basolateral DA-induced depolarization. In contrast to the basolateral side, luminal DA caused depolarization via a D1-like receptor; however the change was less than that for basolateral DA. For further evaluation, 22Na+ flux (J(Na)) was measured to confirm the effect of DA on Na+ transport. Basolateral DA also caused a suppression of J(Na), and this reaction was abolished by domperidone. These results suggested that the basolateral D2-like receptor is mainly responsible for the natriuretic action of DA in rabbit CCD.

Although nasal continuous positive airway pressure (CPAP) is effective in improving nocturnal obstructive apnoea, daytime sleepiness and well-being in patients with obstructive sleep apnoea syndrome (OSAS), not all patients tolerate this treatment. Since optimal CPAP titration is essential to maintain compliance, it is important to elucidate the factors that help to determine the optimal pressure. However, the determinants of the optimal CPAP level are controversial. The subjects comprised 27 Japanese male patients with OSAS who underwent standard polysomnography (PSG), pulmonary function tests, arterial blood gas analysis, cephalometry and CPAP titration. Twenty normal controls also underwent cephalometric analysis. The apnoea-hypopnoea index (AHI), mean oxygen saturation (mean SaO2) and the lowest SaO2 during sleep were found to be 54.7+/-22.6, 89.0+/-5.6%, and 69.7+/-9.0%, respectively by PSG. The mean optimal CPAP was 9.6+/-1.8 cmH2O. The cephalometric angles (SNA, SNB and NSBa) were similar to those found in the control subjects. but MP-H, and PNS-P were significantly longer than those in the control subjects as shown by cephalometry. The optimal CPAP was correlated with the mean SaO2 (P<0.0001), neck circumference (P<0.05) and three cephalometric variables (NSBa: P<0.01, MP-H: P<0.05, PNS-P: P<0.05). Multiple, step-wise, regression analysis showed that the mean SaO2 and NSBa were independent variables that best predicted the optimal CPAP. These variables accounted for 57.5% of the total variance (R2=0.575, P<0.001). Optimal CPAP was closely correlated with oxygen desaturation during sleep. However, the craniofacial structure had additional effects such as an independent factor in determining the optimal CPAP level.

Background: It has been reported that human recombinant erythropoietin (rHuEpo) modulates the sensitivity of the cardiovascular system to angiotensin II (Ang II) or noradrenaline (NA). In the present study, we explored the effect of rHuEpo on the responsiveness of Ang II- or NA-induced cytosolic free calcium ([Ca(2+)]i) mobilization in cultured rat vascular smooth-muscle cells (VSMC)., Methods: [Ca(2+)]i concentrations in VSMC were measured by using the calcium-sensitive fluorescent dye fura-2., Results: The addition of rHuEpo (250 U/ml) alone induced elevation in [Ca(2+)]i, which remained significantly elevated above basal level for at least 60 min in the presence of extracellular Ca(2+). Pre-incubation with specific protein kinase C (PKC) inhibitor calphostin C (1 micromol/l) significantly reduced the peak and the sustained elevations of [Ca(2+)]i. Pre-treatment with rHuEpo for 60 min increased both basal [Ca(2+)]i and the changes in [Ca(2+)]i by Ang II or NA in a dose-dependent manner in the presence of extracellular Ca(2+). The synergistic effects of rHuEpo with Ang II or NA were also retained when VSMC were bathed in the Ca(2+)-free medium after the pre-incubation of rHuEpo. Conversely, they were diminished in the presence of extracellular Ca(2+) combined with intracellular Ca(2+) release inhibitor 8-(NN-diethylamino)octyl-1,3,4,5-trimethoxybenzoate (TMB-8). The synergistic effects of rHuEpo were also diminished by PKC depletion or by PKC inhibitor., Conclusions: These observations suggest that rHuEpo has synergistic effects on Ang II- or NA-induced [Ca(2+)]i mobilization, particularly on intracellular Ca(2+) release, in VSMC. This may be a potential mechanism contributing to hypertension associated with rHuEpo therapy.

The role of glutamate in the N-methyl-4-phenyldihydropyridinium (MPP+) toxicity has been argued in the past decade. However, the effects of glutamate efflux and NMDA antagonist on MPP+-induced dopamine overflow have not been documented. To clarify this, we perfused MPP+ through a microdialysis probe in the striatum of freely moving mature C57BL/6 mice. The 60-min perfusion of 10 and 100 microM MPP+ strikingly increased dopamine levels to 28- and 93-fold of the basal values, respectively. In contrast, an administration of MPP+ did not induce marked glutamate release: the MPP+-perfusion slightly increased the glutamate level at 100 microM, but not at 10 microM. The addition of 100 microM (+)-MK-801 or 200 microM (+/-)-AP-7 to the perfusate did not attenuate MPP+-induced dopamine overflow. The extent of dopamine release only depended on the amount of MPP+ accumulation into the cells. These results indicated that, at least in the striatum, neither glutamate release nor the NMDA antagonist, including (+)-MK-801, could regulate MPP+-evoked dopamine overflow.

Carbolines, azaheterocyclic amines derived from indoleamines, have various biological activities, such as neurotoxicity of beta-carbolines and potent mutagenicity of gamma-carbolines. In this study, structural significance among these carbolines was investigated in relation to the types of cell death, apoptosis and necrosis, using human neuroblastoma SH-SY5Y cells. DNA damage was quantitatively analyzed by a single-cell gel electrophoresis assay. DNA damage was induced by both beta-carbolines, harman and norharman, and gamma-carbolines, 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1) and 3-amino-4-methyl-5H-pyrido[4,3-b]indole (Trp-P-2), in a dose dependent manner. Gamma-carbolines were more potent to damage DNA than beta-carbolines. Alkaline lysis of the cells prevented DNA damage induced by beta-carboline, and pre-treatment of the cells with cycloheximide, an inhibitor of protein synthesis, reduced DNA damage caused by norharman. Morphological observation showed condensed and fragmented nuclei typical for apoptosis, in the cells treated with norharman. Thus, DNA damage induced by norharman was proved to be apoptotic. However, harman, which had a methyl substitution at the position 1, might induce necrosis in the cells. On the other hand, gamma-carbolines, Trp-P-1 and Trp-P-2, directly damaged DNA. Thus, the nitrogen atom at the gamma-position and/or an amino group in carboline structure would be required to induce the direct DNA cleavage.

A 78-year-old woman committed double suicide with a bolus injection of 1 g of lidocaine hydrochloride. The tissue distribution of lidocaine in this fatal poisoning was investigated using an improved gas chromatographic method. The blood level was 42 microg/ml and the brain concentration was 70 miccro/g. Thus, the cause of death in this case was clearly diagnosed as lidocaine overdosing. The blood level of 42 microg/ml was higher than that calculated using the standard pharmacokinetic parameters. Lower blood/tissue ratios were also detected compared with the data described in the literature. These results indicated that the cardiac failure should have occurred immediately after the lidocaine injection. The present data show the distribution of lidocaine after acute death due to overdosing.

Multiple myeloma causes various renal injuries by direct invasion of myeloma cells, AL amyloidosis and hypercalcemia. Hypercalcemia induced by myeloma has been thought to be a result of local osteolysis. Recently, however, it was noted that no significant difference existed in the degree of bone-destruction between hypercalcemic and normocalcemic multiple myeloma. The exact mechanisms of hypercalcemia induced by multiple myeloma remain unconfirmed. In the present study, we report a 70-year-old man, suffering from acute renal failure due to multiple myeloma and severe hypercalcemia. While the serum PTH level was low, PTHrP was markedly increased. Bone scintigraphy implied systemic increase in bone turnover in addition to cold spots corresponding to punched out lesions on bone Xp. After the intravenous administration of bisphosphonate, hypercalcemia and hot accumulation on bone scintigraphy were improved while the PTHrp level and bone destruction by myeloma cells were not improved. The present case suggests involvement of PTHrP in hypercalcemia of multiple myeloma.

To evaluate the circadian pattern of blood pressure (BP) and the effects of nasal continuous positive airway pressure (CPAP) on patients with obstructive sleep apnea (OSA), we examined 24-hour BP in 38 male OSA patients with and without nasal CPAP. We measured the BP at 30-min intervals during daytime (800 to 2200) and nighttime (2200 to 800) hours. A "dipper" was defined as a patient who showed an average reduction of at least 10 mm Hg systolic and 5 mm Hg diastolic between daytime and nighttime values. The subjects were predominantly "non-dipper" (22 of 38 patients, 58%). Daytime hypertension (>160/95 mm Hg) was present in 11 of 38 patients (4 "dippers" and 7 "non-dippers"). After nasal CPAP treatment for 3 days, the average BP decreased significantly during the day and night in all subjects (p<0.05). Fifteen of 22 subjects who were "non-dippers" before treatment reversed to become "dippers." And daytime hypertension was detected in only 5 of these patients during nasal CPAP treatment (4 "dippers" and 1 "non-dipper"). These results showed that the "non-dipper" status was common in patients with OSA, and that nasal CPAP restored the normal circadian "dipper" pattern. We suggest that nasal CPAP may contribute to an improved prognosis in patients with OSA because of a reduction in cardiovascular risk factors in "non-dipper" with severe OSA.

Peripheral bronchial carcinoids sometimes arise as single solid or nodular lesions in the periphery of the lung. We encountered a 74-year-old Japanese male with bronchial carcinoids that were widely disseminated throughout the lung parenchyma. Pulmonary function tests revealed mild airflow obstruction. A metastatic process was ruled out from primary malignancy and a histological examination revealed findings consistent with a peripheral bronchial carcinoid. Based on these findings, we concluded that this patient had a primary multifocal peripheral bronchial carcinoid. An immunohistochemical examination revealed immunoreactivity for chromogranin A and bombesin. The present case appears to be an unusual case of diffuse multifocal peripheral bronchial carcinoid, confirmed by immunohistochemistry.

Historical demography as a separate discipline came into existence when family reconstruction was first developed for the analysis of a pre-transition population. This paper assesses the significant achievements made in this field of population studies since then. Attention is also paid to equally significant findings obtained from aggregative analysis based on back projection, and to a large body of research results for the period of the demographic transition. In the last part of the paper, new research directions are discussed. Data issues as well as methodological ones are raised. Special attention is given to newly emerging Asian historical demography where different source materials require different methods and techniques, which in turn are expected to broaden the scope of the so far disproportionality fertility-oriented field. Finally, discussions are extended to economic, cultural and institutional aspects of the subject, with a plea not to isolate demographic analysis from other branches of historical research.

AIDS can affect many parenchymal organs but the renal involvement is of vital value for patient's prognosis. Sonography can easily analyse most of all renal insult even in those patients without symptoms.

We previously reported that mean pulmonary arterial pressure (Ppa) during pulsatile flow exceeded that for steady flow when flow was greater than the normal resting value and speculated that this was due to irregularities of the flow profiles in precapillary vessels, mainly the larger arteries. From this we hypothesized that neither mean microvascular pressure nor the rate of fluid filtration would be affected by flow pulsatility. We therefore compared the effects of steady vs. pulsatile flow on the double-occlusion pressure (Pdo) and on edema formation (rate of weight gain) in zone 3 rabbit lungs. Excised left lungs (n = 19) were perfused with Tyrode solution and ventilated with an end-expiratory pressure of 2.5 cmH2O. A diaphragm pump generated pulsatile flow with a stroke volume of 1.0 ml (approximately 0.8 the normal resting value for rabbit left lung). Nonpulsatile flow was generated by raising an arterial reservoir. Flow rate was set at 100 or 400 ml/min (approximately 0.4 or 1.6 x the normal resting cardiac output, respectively). Vascular pressures (referenced to the bottom of the lung) were measured after ventilation, at end expiration, was interrupted. Pdo values were obtained in random order at 15 time points that were evenly distributed within the pulse cycle, averaged across pulses to obtain the mean capillary pressure profile, and then averaged over time. At the lower flow of 100 ml/min, mean Ppa and Pdo were slightly lower (3-4%) during pulsatile compared with nonpulsatile conditions. At the higher flow of 400 ml/min, mean Ppa was higher under pulsatile conditions (13%), whereas downstream the mean Pdo values were equal.(ABSTRACT TRUNCATED AT 250 WORDS)

We compared the effects of pulsatile vs. nonpulsatile flow (Q) on pulmonary arterial pressure (Ppa)-Q relationships in zone 3 over wide ranges of pulse rate, stroke volume (SV), and Q. Excised left lungs of rabbits (n = 15) were perfused with tris(hydroxymethyl)aminomethane-buffered Tyrode solution containing 4% dextran, 1% albumin, and 10 mg/l of indomethacin and were ventilated with room air. Pulsatile Q was generated by a diaphragm pump delivering SV of 0.5, 1, or 2 ml (representing approximately 0.3, 0.6, and 1.2 times, respectively, the normal resting SV for rabbit left lung) and adjusting the pump frequency. Nonpulsatile Q was generated by raising an arterial reservoir to the required height. Mean pulmonary arterial (Ppa) and left atrial pressures were measured at end exhalation (positive end-expiratory pressure = 2.5 cmH2O) near the tips of the perfusion cannulas and were referenced to the lung base. Left atrial pressure was held constant at 7 cmH2O.Q was alternated between pulsatile and nonpulsatile, increasing Q stepwise from 100 to 600 ml/min (Q from approximately 0.3 to 2 times the normal resting Q for rabbit left lung), after which Q was reduced stepwise back to initial values. For the smallest SV there were no differences between Ppa-Q curves under pulsatile and nonpulsatile conditions. At the largest SV, Ppa was greater during pulsatile than nonpulsatile Q at Q > 100 ml/min. The slopes of the Ppa-Q curves were greater during pulsatile Q at the two larger SV values. These results can be explained by increasing Q turbulence and less ideal velocity profiles at higher peak Q resulting from the effects of rapidly changing inertial forces.

Ten patients with Ramsay Hunt syndrome underwent magnetic resonance (MR) scans. In many examinations, abnormal enhancement of the 7th nerve in the internal acoustic meatal segment through the mastoid segment was observed. Out of seven patients with cochlear and/or vestibular symptoms, only one showed abnormal enhancement of the 8th nerve, in addition to the 7th. The other 6 patients showed the same findings as in Bell's palsy, showing no enhancement of the 8th nerve. This suggests that clinical symptoms have no relation to the results of MRI. Enhanced MRI is the most sensitive means of making differential diagnoses between Hunt's syndrome and tumors, but it is impossible to detect all lesion sites corresponding to the symptoms in Hunt's syndrome.

The method of detecting diabetes mellitus and estimating the diabetic control status in patients with Bell's palsy, and the effect of high-dose steroid therapy for Bell's palsy accompanied by diabetes were investigated. From October 1987, hemoglobin A1c (HbA1c) was introduced to detect diabetes in 288 out of 372 patients with Bell's palsy, as a screening test for DM. Thirty-six diabetics with complete facial palsy were treated by high dose steroid therapy as described by Stennert. Hemoglobin A1c was useful in diagnosing diabetes and in assessing the diabetic control. Many patients under diabetic therapy kept their diabetes under good control. In cases of complete palsy, high-dose steroid therapy, at a cure rate of 97.4%, was highly effective in treating diabetes-accompanied Bell's palsy.

The etiology of Bell's palsy is still obscure and its treatment remains controversial. As a conservative treatment for Bell's palsy, Stennert developed a new treatment method for the purpose of improving microcirculation, and reported an extremely high cure rate of 96%, drawing a great deal of attention. However, since the electrophysiological findings and side effects in these patients were not described satisfactorily in his report, this method has not yet come into wide clinical use. In the present study the efficacy of Stennert's method was assessed by electrophysiological examination in patients, and was compared with patients treated by conventional methods. The subjects of this study were 157 patients with Bell's palsy who were treated with a modification of Stennert's method between September 1987 and August 1990. The treatment protocol for the modified Stennert's method was as follows: hydroxyethyl starch 40 with 20% mannitol is given instead of Dextran 40 and prednisolone is stopped depending on the findings of electrical examinations. Fifty-three patients with Bell's palsy treated by the conventional method used in our clinic between November 1983 and August 1987 were used for the control group. The most remarkable difference between these two methods was the initial dose of prednisolone. In the group treated by the modified Stennert's method, 111 patients (70.7%) showed complete recovery within 1 month, and 154 patients presented (98.1%) showed complete recovery within 6 months, 3 cases presented slight sequelae. In the conventional treatment group, on the other hand, only 2 patients (3.8%) recovered within 1 month, and 43 patients (81.0%) recovered within 6 months.(ABSTRACT TRUNCATED AT 250 WORDS)

The etiology of Bell's palsy is still obscure, but the hypothesis that hypoxia and compression of the nerve induced by edema in the Fallopian canal are the main causes of Bell's palsy is widely accepted. Tojima (1988) reported that the motor nerve conduction velocity (MCV) gradually decreased as degeneration of the nerve fibers progressed in Bell's palsy. The majority of facial nerve fibers are myelinated, and the greater the fiber diameter, the faster the conduction velocity. For this reason, Tojima suggested that Wallerian degeneration in Bell's palsy would begin from the thicker myelinated fibers. The measurement of MCV, however, reveals only the activities of the fastest velocity motor nerve fiber in the nerve trunk. This weak point can be resolved by measurement of the distribution of nerve conduction velocities (DNCV), which was introduced by Hopf in 1962 as the collision method. In the present report, the DNCV of facial nerve was measured using the collision method to estimate the distribution of the diameter of nerve fibers in normal subjects and patients with Bell's palsy and to elucidate the pathophysiology of Bell's palsy. The subjects were 14 normal adults (19 measurements) and 14 patients with Bell's palsy who visited our university clinic within 7 days to 18 days after onset, with no other complications such as diabetes. Results obtained are as follows. 1) The mean DNCV in 14 normal subjects (19 measurements) was unimodal, showing a peak at 20 to 22 m/s. 2) In DNCVs of patients with Bell's palsy, loss of thicker fibers with faster conduction velocity was recognized (11/14, 79%).(ABSTRACT TRUNCATED AT 250 WORDS)

The purpose of the present study was to analyse the quantitative relationship between the property of food and the jaw-closing muscle activities as well as how the periodontal afferents participated to establish such a relationship. The following experiments were performed in the urethane anesthetized rabbits: 1) EMG activities of the masseter muscle during the cortically-induced rhythmical jaw movements (CRJMs) before and during chewing rubber strips with different hardness were compared each other. 2) Effects of combined sections of the maxillary and the inferior alveolar nerves on the masseteric EMG responses during chewing a strip were analysed. 3) Effects of the transection of the trigeminal spinal tract on the above masseteric responses were also analysed. The results were as follows: 1) The masseteric activities during the CRJMs differed depending on the site of the cortical stimulation. According to the level of the masseteric activity, CRJMs were divided into two types; one was the opening-dominant jaw movement (ODJM) with small masseteric activity, and the other was the closing-dominant jaw movement (CDJM) with large masseteric activity. In any CRJMs, the masseteric activity became larger during the insertion of a strip, but the increment was more prominent for the ODJM. The rate of increment of the masseteric activity became larger with the hardness of the strip. 2) After the periodontal deafferentation, the rate of increment of the masseteric activity during chewing a strip was remarkably reduced, especially in the ODJM. On the contrary, deafferentation was less effective to that in the CDJM. 3) The effects of the transection of the trigeminal spinal tract were similar to those of the trigeminal deafferentation. From these results, the following conclusions were obtained: 1) The masseteric activity was facilitated with the hardness of the strip. Furthermore, the rate of increment of the masseteric activity during chewing a strip differed depending on the masseteric activity induced before the strip insertion. 2) Periodontal afferents played an important role in the above facilitatory effect, especially when the masseteric activity was small. 3) The contribution of the periodontal afferents which descended through the trigeminal spinal tract was suggested to be involved in the facilitatory response of the masseter muscle during chewing a strip.

The biochemical activities of 8 lysosomal acid hydrolases in leukemic cells from 48 patients were examined. Characteristic alterations were found in alpha-mannosidase, beta-galactosidase and N-acetyl-beta-glucosaminidase activities of leukemic cells. The level of alpha-mannosidase activity was much higher in myelo(mono)genous leukemias (AML, AMoL, AMMoL, CML and CMMoL) than in lymphogenous ones (ALL, T-cell leukemia, hairy cell leukemia and CLL) without exception. The beta-galactosidase activity also differed as a result of alpha-mannosidase, except in T-cell leukemia. In T-cell leukemia it was within the range of normal lymphocytes, but in the other lymphogenous leukemias it was significantly below normal. N-acetyl-beta-glucosaminidase activity in myelo(mono)genous leukemic cells was above the range of normal granulocytes. The changes in these enzyme levels were consistent. The lymphocytic or myelocytic nature of three cases of acute undifferentiated leukemia could be determined by enzyme studies. In two cases it was lymphocytic and in one it was myelocytic. The enzymatic abnormalities were also found in morphologically mature neutrophils from patients but not only chronic types (CML, CMMoL) but also acute types (AMoL, AMMoL) of leukemias, and were similar to those of their respective leukemic cells. Analysis of lysosomal enzymes (at least three of those mentioned above), can elucidate one of the biochemical properties of leukemic cells and may be valuable in the differentiation of leukemias.

We investigated the present status concerning the performance of examinations of facial nerve function for facial palsy, based on statistics obtained from the project supported by a Grant-in-Aid for Co-operative Research (A) from the Ministry of Education. The project is called An Epidemiological and Clinical Study on the Idiopathic Facial Palsy. In an analysis of the questionnaire "individual investigation card for idiopathic facial palsy" obtained from 28 medical facilities throughout Japan between 1984 and 1986, the outline of the examinations performed for peripheral facial palsy was examined.

The purpose of this study is to reveal the relationship between the head position, and the neck and head muscles. At 4 head positions, the activities of masseter, anterior temporal, anterior digastric, sternocleidomastoid and trapezius muscle of ten normal subjects standing straight were investigated electromyographically with surface electrodes during voluntary maximal clenching in centric occlusion. Head positions were right tilting, left tilting, up-right and natural head position. The results obtained were as follows; 1. During head tilting, the activities of anterior digastric and sternocleidomastoid muscle on the tilting side were increased, the activities of masseter and trapezius muscle on the opposite side of the tilting side were increased, the activity of the anterior temporal muscle did not vary from the activity during up-right head position. 2. During natural head position, only the activity of sternocleidomastoid muscle on the natural tilting side was increased.

The isoenzyme profiles of hexosaminidase in leukemic cells from 39 patients were examined with DEAE-Sephadex chromatography. There was a clear difference in the isoenzyme composition between normal lymphocytes and granulocytes. In acute non-T/non-B lymphocytic leukemia (ALL) a characteristic alteration was found in the intermediate forms of hexosaminidase (Hex I), which was significantly higher than those of normal lymphocytes (p less than 0.001). Subtypes of Hex I (Hex i1-i4) and the heterogeneity of their abnormal expression in ALL was demonstrated. There was no type-specific alteration of the isoenzyme profiles in T-cell leukemia. Leukemic cells of acute myelocytic leukemia (AML) had significantly higher Hex P component than granulocytes (p less than 0.01) and ALL cells (p less than 0.01). The increase of Hex P was evident in childhood AML. There was a significant difference in Hex P level between childhood AML and adult myelo(mono)genous leukemia (p less than 0.001). Chronic myelo(mono)genous leukemia showed similar isoenzyme compositions to normal granulocytes. The isoenzyme profiles in acute undifferentiated leukemia differed from those in other types of leukemia. Isoenzyme analysis might be useful for probing the nature and the intrinsic biochemical abnormality of leukemic cells.

For purpose of evaluating the characteristic of electromyographic activities of masticatory muscles with front or molar tooth loss, electromyographic activities of masticatory muscles and mandibular movements during tooth tapping and gum chewing were investigated in each group of tooth loss, and were compared with those of control group. The results were as follows. 1. In reference to the group with front tooth loss, 1) On tooth tapping, each S.D. of the time parameters of electromyographic activities of jaw closing muscles especially masseter and posterior temporalis was small, and that of jaw opening muscle was large. 2) On gum chewing, offset of jaw closing muscles' activities especially masseter and anterior temporalis were delayed. 3) On both tooth tapping and gum chewing, there was no difference in mandibular movements from control group. 2. In reference to the group with molar tooth loss, 1) On both tooth tapping and gum chewing, each S.D. of the time parameters of electromyographic activities of jaw closing muscles was large. 2) On tooth tapping, S.D. of opening ratio was large. 3) On gum chewing, both S.D. of chewing cycle and opening ratio were large.