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Biomedical subjects

T Sakaguchi

Publications and source records attributed to T Sakaguchi.

At least 217 records · Page 12Linked to original sources
PubMed1991

Composite reconstruction for chest wall and scalp using multiple ribs-latissimus dorsi osteomyocutaneous flaps as pedicled and free flaps.

A composite flap is presented based on the latissimus dorsi myocutaneous unit together with the underlying ninth to eleventh ribs. Three patients are presented. In two, a full-thickness chest-wall defect was present. In one, a full-thickness scalp and cranial defect was present. Use of the composite osteomyocutaneous latissimus dorsi free flap as a pedicled flap in two patients and as a free flap in one patient resulted in successful definitive reconstruction in all with no complications. This procedure necessitates no transplantation of soft tissue prior to bone grafting to maintain local vascularity, so the simultaneous one-stage reconstruction of an osseous-soft-tissue defect becomes possible easily.

Adult↗
PubMed1991

Congenital factor VII abnormality discovered in an infant at a routine checkup.

Congenital coagulation factor VII abnormality in an infant was first discovered because of a decreased normotest value at a routine health checkup at the age of 1 month. No bleeding tendency had been noticed. The normotest value did not respond to an administration of vitamin K. The prothrombin time (PT) was prolonged, and the activated partial thromboplastin time (A-PTT) was in the normal range. Factor VII activity was extremely low, whereas the level of factor VII antigen was relatively low. These data indicate that the propositus is a factor VII reduced variant, a rare variant of congenital factor VII deficiency. The propositus and her brother are homozygotes, and her parents and sister are heterozygotes.

Blood Coagulation Tests↗
PubMed1991

Significance of prenatal diagnosis in a patient with a huge neck tumor.

Due to the great advancements in fetal ultrasonography, the number of prenatal diagnoses are increasing, greatly contributing to improved neonatal surgery. It is now relatively easy to detect huge fetal cystic masses, and we have experienced three cases with a huge neck tumor detected in utero, one case with teratoma and two cases with cystic hygroma. Each case was complicated by neonatal asphyxia, and the neonate needed resuscitation by means of endotracheal intubation. The infant with teratoma unfortunately died of respiratory distress due to compression of the trachea before a perinatal team could be organized. Although the remaining cases with cystic hygroma were treated by a perinatal team, one died 19 hours after birth and the other has survived with the aid of endotracheal intubation in the hospital for three years. In addition, all four cases of cystic hygroma detected antenatally in our institute, which were not delivered, also had fetal hydrops which suggested a general lymphatic derangement. Cystic hygroma detected in utero is considered to be different from that detected after birth, since the former is associated with genetic lymphatic derangement. Prenatal diagnosis enables such patients to survive the perinatal period, but may not improve the prognosis of fetal cystic hygroma so much.

Adult↗
PubMed1991

[Effects of lumbar epidural anesthesia on brainstem auditory response].

Auditory brainstem responses (ABR) are used increasingly to monitor the integrity of neural pathways in anesthetized patients. To evaluate the effect of epidural anesthesia on the central nervous system, we studied the effects of lumbar epidural anesthesia with lidocaine on the ABR in 10 patients. The seven peak latencies (waves I-VII) and amplitudes (waves I-VII) of the ABR were recorded before and 15 min after epidural anesthesia. Peak latencies of waves III, IV, V, VI, VII increased after epidural anesthesia compared with control values. Amplitude of waves II only decreased significantly following epidural anesthesia compared with control values. We further compared the interpeak latencies to investigate the brainstem transmission. Interpeak latencies (I-II, II-III, III-IV, IV-V, V-VI, VI-VII) were unchanged from the control values except waves VI-VII interval. Interpeak latencies of every second peak (II-IV, IV-VI, V-VII), of every third peak (II-V, III-VI, IV-VII), of every forth peak (I-VI, II-VII), of every fifth peak (I-VII) increased after epidural anesthesia compared with control values. The data obtained in the study demonstrated that lumbar epidural anesthesia with lidocaine prolonged the interpeak latencies of ABR. Considering that the waves of ABR are related to anatomically distinct sites in the auditory pathway (I; Acoustic nerve, II; Cochlear nucleus, III; Superior olivary complex, IV; Lateral lemniscus, V; Inferior colliculus, VI: Medial geniculate body, VII; Auditory radiation), the delay in the latencies of ABR seems to be present in the time intervals which involve more than two or three synaptic transmissions.

Anesthesia, Epidural↗
PubMed1990

Duration-dependent effects of repeated restraint stress on cortical projections of locus coeruleus neurons.

Using electrophysiological techniques, changes in noradrenergic fiber innervation in the cerebral cortex following repeated stress (restraint in a small cage for either 1 or 6 h daily) were examined by quantifying the density of cortical terminal axons of locus coeruleus (LC) neurons in the rat. After termination of the stress treatment, the single-unit activity of LC neurons was recorded extracellularly under urethane anesthesia, and antidromic activation from 7 cortical points covering nearly the entire cerebral cortex was examined. The percentage of LC neurons activated anti-dromically from the medial frontal cortex was higher in the animals stressed for 1 h daily for 2 weeks. In contrast, the percentage of LC neurons activated antidromically from the cerebral cortex decreased in the animals who received 6 h stress for 2 weeks. These results suggest that stress can cause dual effects, either sprouting or retraction of cortical LC axons depending upon the duration of stress treatment.

Animals↗
PubMed1990

Gastrin-17 injected into the hypothalamic paraventricular nucleus can induce gastric acid secretion in rats.

Injections of picomolar quantities of gastrin-17 into the hypothalamic paraventricular nucleus increased gastric acid output in anesthetized rats. The response was dose-dependent, and it was blocked by atropin and by vagotomy. The same doses, injected intravenously, intraventriculary or into sites far from the nucleus, did not increase the output. Cholecystokinin-8 injected into the nucleus had no effect on the acid output.

Animals↗
PubMed1990

Assessment of tubular function in neonates using urinary beta 2-microglobulin.

Renal proximal tubular function was assessed in neonates by measuring urinary beta 2-microglobulin (beta 2M) concentrations on days 1, 4, 7, 14 and 28. Values were elevated in stable preterm low-birthweight (LBW) neonates but not in stable term LBW neonates, suggesting that proximal tubular maturation is related to gestational age rather than birthweight. The urinary beta 2M was significantly increased on day 1 in neonates with the meconium aspiration syndrome but was not significantly different from normal subsequently. This indicated that although the proximal tubular cells may be susceptible to perinatal hypoxia, they maintain a remarkable capacity to recover in a relatively short period. Neonates with transient tachypnoea of the newborn had normal urinary levels of beta 2M indicating their renal tubular function was not impaired.

Apgar Score↗
PubMed1990

Immediate protection of mice from lethal wild-type Sendai virus (HVJ) infections by a temperature-sensitive mutant, HVJpi, possessing homologous interfering capacity.

Protection of mice from lethal Sendai virus (HVJ) infections by a temperature-sensitive mutant, HVJpi, which was isolated from a carrier culture, was studied. HVJpi had a strong interfering capacity with the replication of virulent wild-type virus in LLCMK2 cells. When a high dose of HVJpi (3.0 x 10(7) CIU) was inoculated intranasally into mice, the mice showed neither illness nor lung lesions but gained significant resistance against the challenge of virulent wild-type virus (18 LD50) immediately after inoculation. In contrast, the mice inoculated with a lower dose of HVJpi (8.2 x 10(5) CIU) did not show the immediate resistance but became immune several days after inoculation. Time courses of the virus replication in the lung revealed that the replication of wild-type virus was strongly suppressed to about 1/1000 by the simultaneous infection with a high dose of HVJpi, thus resulting in minimizing the lung lesions and survival of all the mice infected. Neither interferon nor natural killer cells appeared to play a major role in the immediate immune status by HVJpi, since no difference was observed in protection of mice simultaneously infected with wild-type virus and HVJpi in spite of pretreatment of the mice with anti-interferon and anti-asialo GM1 antibodies as compared with that of the untreated doubly infected mice. On the other hand, it was suggested by analysis of viral polypeptides synthesized in the lung of infected mice by Western blotting that the early stage of replication of wild-type virus in the lung was inhibited mainly by the interfering capacity of HVJpi. These results indicate that HVJpi is an unique virus mutant which is capable of protecting mice from lethal Sendai virus infections by its interfering capacity immediately after inoculation and then by the induction of virus-specific immune responses.

Animals↗
PubMed1990

Gastric vagal functional distribution in the secretion of gastric acid produced by sweet taste.

The sweet signal pathway relevant to lingual control of gastric acid secretion was examined in bilaterally adrenalectomized rats. The increase in the acid output after lingual glucose application was completely blocked by prior section of both sides of the vagus nerve at the cervical level. However, the reduction in the acid output showed no laterality following vagotomy on either side. At the subdiaphragmatic level, the acid response was mainly suppressed by section of the dorsal vagus trunk. Both sides of trunk vagotomy abolished the acid response. These results suggest that the sweet signal evoking gastric acid secretion has a specific pathway from the tongue to the stomach, and that there is functional laterality in this pathway in the visceral cavity.

Adrenalectomy↗
PubMed1990

RNA synthesis and processing in the gerbil brain after transient hindbrain ischaemia.

Ribonucleic acid (RNA) synthesis was investigated in gerbils subjected to 15 min transient hindbrain ischaemia using [2-14C]uridine autoradiography. Distribution of synthesized RNA in the subcellular fraction of the tissue was detected by differential centrifugation and density gradient separation using Whittaker's method. In [2-14C]uridine autoradiography, uptake of the tracer into the RNA fraction was not reduced after transient ischaemia. Distributional analysis of [2-14C]uridine in the subcellular fractions revealed that tracer activity in the P3 (microsomes) fraction decreased in the ischaemic regions and tended to decrease in the P4 (ribosomes) fraction, although not significantly. Tracer activity in the P1 (nuclei and cell debris) and P2 (mitochondria, myelin and nerve ending particles) fractions did not decrease. These results indicate that RNA synthesis in the nuclei is not inhibited by ischaemia, but RNA processing is disturbed by the level of the transport. Modification of RNA synthesis and processing by transient ischaemia may influence protein synthesis.

Animals↗
PubMed1990

Inhibition of muscarinic-coupled phosphoinositide hydrolysis by N-methyl-D-aspartate is dependent on depolarization via channel activation.

The intent of this work was to elucidate the mechanism by which N-methyl-D-aspartate (NMDA) receptor agonists inhibit a second messenger system, namely, the stimulation of phosphoinositide (PI) hydrolysis activated by muscarinic cholinergic receptor agonists. NMDA inhibited cholinergic stimulation of PI hydrolysis in a dose- and time-dependent manner. NMDA exerts this effect indirectly through channel activation, because both MK-801 and N-[1-(2-thienyl)cyclohexyl]piperidine (TCP) prevented this action. Prevention of the NMDA effect by removal of sodium, but not calcium, from the incubation buffer suggested that depolarization may be the responsible mechanism. Depolarization alone proved sufficient to inhibit cholinergic activation of PI hydrolysis, because both veratridine and an elevated extracellular potassium level inhibited cholinergic stimulation of PI hydrolysis. The effect of NMDA appeared to require sodium flux through NMDA channels rather than through voltage-dependent sodium channels, because tetrodotoxin failed to inhibit the effect of NMDA. In correlative electrophysiologic experiments, NMDA profoundly inhibited evoked excitatory postsynaptic potentials and population action potentials of CA1 neurons, an effect almost certainly due to depolarization. The dose and time course of the electrophysiologic effects correlated well with the biochemical effects. Taken together, the data support the assertion that NMDA receptor activation inhibits PI hydrolysis by depolarization mediated by sodium flux through NMDA channels.

Animals↗
PubMed1990

Angiographic demonstration of acute phase of intracranial arterial spasm following aneurysm rupture. Case report.

A case documenting the acute phase of intracranial arterial spasm following rupture of an aneurysm arising from the left internal carotid artery is reported. The patient deteriorated due to recurrent hemorrhage while undergoing angiography 12 hours after the initial aneurysm rupture. The acute deterioration was accompanied by dilatation of the ipsilateral pupil and occurred during injection of contrast material. There was delayed filling of the middle cerebral artery complex along with this narrowing. The arterial narrowing was confirmed to have completely disappeared on an angiographic series performed 14 minutes after the first series of films. The etiology of the acute vasospasm is discussed.

Aneurysm↗
PubMed1990

An enzyme immunoassay for galactosyltransferase isoenzyme II, and its clinical application to cancer diagnosis.

In this "sandwich"-type enzyme immunoassay of galactosyltransferase isoenzyme II (GT-II), we used the monoclonal antibody MAb 3872 previously established and characterized to be specific for GT-II. Plastic beads coated with MAb 3872 were incubated with serum and buffer, washed, then incubated with MAb 3872 conjugated with horseradish peroxidase and again washed. Peroxidase activity remaining on the beads was measured by color development with o-phenylenediamine. The assay standard curve was linear from 0 to 150 kU/L. Inter- and intra-assay CVs were less than 9% and less than 7%, respectively. Mean GT-II values for 370 normal controls were 6.8 (SD 3.4) kU/L with no significant sex-, smoking-, or blood-type-related differences. We also assayed serum from patients with 11 different cancers or with matched benign diseases. The diagnostic sensitivity of GT-II for liver and esophageal cancer was 0.91 and 0.72, respectively, apparently higher than for carcinoembryonic antigen (CEA) or alpha-fetoprotein. GT-II and CEA concentrations in sera were not correlated. Evidently this assay may be useful as a cancer diagnostic test to supplement existing serological methods.

Adult↗
PubMed1990

On the changes in peripheral red cells in mice exposed to vinyl chloride monomer.

The diseases known as the Vinyl Chloride Monomer (VCM) Syndrome include hepatic angiosarcoma, acroosteolysis and Raynaud's phenomenon. These, however, are known to be clinically recognizable from several to over 10 years after the actual exposure to VCM. By fluorescence microscopy the authors examined smeared samples of peripheral blood obtained from vinyl chloride workers, and observed the existence of basophilic stippled erythrocytes (BSE). In this paper, we report the changes of peripheral red cells during VCM exposure tests on mice. These changes in the peripheral blood could be observed as early as 24 hours after the start of the VCM exposure at higher concentrations, and in 72 hours even at comparatively lower VCM levels of 30 to 40 ppm. The tests have also confirmed that the rate of emergence of BSE differs according to the level of VCM and to the duration of VCM exposure.

Animals↗
PubMed1990

Ventromedial hypothalamic lesions attenuate responses of sympathetic nerves to carotid arterial infusions of glucose and insulin.

The effects of intracarotid injections of glucose and insulin on the sympathetic firing of nerves to brown adipose tissue were measured in rats. The injection of glucose into the carotid artery of anesthetized rats increased the firing of nerve filaments from the sympathetic nerves which innervate brown adipose tissue. Injection of kainic acid into the ventromedial nucleus 6-9 days prior to the measurement of nerve recordings reduced the stimulatory effect of glucose by 60 percent. In contrast to the stimulation by glucose, injection of insulin into the carotid artery reduced the sympathetic firing rate of nerves to brown adipose tissue. Kainic acid destruction of neurons in the ventromedial hypothalamus also attenuated this effect by 40 percent. These experiments are consistent with the hypothesis that changes in the arterial concentration of glucose and insulin may modulate the firing rate of sympathetic nerves to brown adipose tissue, and that this effect is mediated, in part, by the ventromedial hypothalamus.

Adipose Tissue, Brown↗
PubMed1990

Therapeutic dilemmas associated with antenatally detected ovarian cysts.

Fifteen instances of ovarian cysts detected antenatally are reported. Seven cysts more than 5 centimeters in diameter were treated surgically because of clinical signs, such as palpable abdominal mass, vomiting and abdominal distension. Seven cysts less than 5 centimeters in diameter, and one cyst more than 5 centimeters in diameter began to regress spontaneously within six months after birth. Because the pathophysiologic nature of neonatal ovarian cysts has not been elucidated and because the borderline between physiologic and pathologic factors is still unclear, we propose a more conservative approach in the management of neonatal ovarian cysts to avoid unnecessary operations.

Clinical Protocols↗
PubMed1989

Effect of norepinephrine, serotonin and tryptophan on the firing rate of sympathetic nerves.

The firing rate of sympathetic nerves innervating interscapular brown adipose tissue (IBAT) has been recorded following microinjection of monoamines into the ventromedial (VMN) and paraventricular nuclei (PVN). Microinjection of norepinephrine (10 nmol) into the paraventricular nucleus produced a biphasic pattern in the firing rate of the sympathetic efferent nerves to IBAT. There was an initial dose-related 20% inhibition of firing rate followed 2 min later by 10% increase above control. When 10 times as much norepinephrine was injected into the ventromedial hypothalamus, there was a small 5% decrease in firing rate and a later significant dose-related increase in firing rate. These effects of norepinephrine were blocked by phentolamine, an alpha-adrenergic blocking drug, but not by propranolol, a beta-adrenergic blocking drug. Injection of serotonin into the paraventricular nucleus produced a short-lived but significant increase in firing rate of sympathetic nerves to brown adipose tissue. Comparable amounts of serotonin injected into the ventromedial nucleus produced a similar magnitude of increase in firing rate which lasted longer. There was a clear dose-response effect of serotonin injected into the PVN, but a much less impressive response when serotonin was injected into the VMN. The response to injections of tryptophan in both the VMN and PVN was similar to those seen with serotonin. When serotonin or tryptophan were injected into the PVN and VMN simultaneously, there was a synergistic increase in sympathetic firing rate. These data are consistent with the hypothesis that both norepinephrine and serotonin can modulate sympathetic firing rate through interaction with neurons in either the VMN or PVN.

Action Potentials↗