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Biomedical subjects

H Nagasaka

Publications and source records attributed to H Nagasaka.

At least 19 recordsLinked to original sources
PubMed2003

Two cases with transient lipoprotein lipase (LPL) activity impairment: evidence for the possible involvement of an LPL inhibitor.

UNLABELLED: Two independent severe hypertriglyceridemic infants with transiently impaired lipoprotein lipase (LPL) activity were observed and the causes were explored. Both infants were female, born prematurely with low birth weight and developed hypertriglyceridemia (Fredrickson type V hyperlipidemia: high VLDL and low LDL/HDL) a few months after birth. While mass levels of their post-heparin plasma LPL and apoprotein C-II (apo C-II), a physiological activator of LPL, were normal, their post-heparin plasma LPL activities were remarkably impaired. Both of their mothers' post-heparin plasma LPL activities were slightly or moderately impaired as well, without a decrease in the LPL mass level. No mutations in the genes for LPL and apo C-II were detected in either patient. In an in vitro study with their serum at onset, we could not detect any distinct circulating inhibitors for LPL. There was no data supporting infection or autoimmune diseases, which might have an impact on LPL activity, during the follow-up period. Levels of their plasma triglyceride (TG) and total cholesterol (TC) were decreased quickly by a dietary intervention with medium-chain triglyceride (MCT) milk and kept normal even after stopping the intervention at around age 1 year. However, their low post-heparin LPL activity persisted and returned to normal at around age 2 years. Their low HDL cholesterol levels persisted even after recovery of the TG and TC levels, although lecithin:cholesterol acyltransferase (LCAT) and cholesterol-ester-transfer protein (CETP), two key enzymes of HDL metabolism, were normal throughout the course. The exact reasons why their post-heparin LPL activities were impaired for a certain period and why their HDL cholesterol levels have remained low are still unclear. CONCLUSION: Transiently impaired LPL activity with no defect in LPL enzyme induced severe hypertriglyceridemia in infants. The transient occurrence of inhibitor(s) for LPL was proposed.

Child↗
PubMed2002

Intramucosal naevus with pseudoepitheliomatous hyperplasia in the gingiva: a case report.

This article describes the unusual case of an intraoral pigmented naevus with pseudoepitheliomatous hyperplasia of the gingiva. A 62-year-old man presented with an almost coal-black pigmented and partly white, spotted, dome-shaped swelling on the lingual gingiva of the mandible. Histologically, the lesion consisted of clusters of round-shaped naevus cells containing melanin granules, reactive with both S-100 immunohistochemical stain and Masson-Fontana silver stain, and pseudoinvasive squamous nests, reactive with cytokeratin. The pathogenesis of the present lesion and problems encountered in its differential diagnosis are discussed.

Basal Cell Carcinoma↗
PubMed2001

Circulating matrix metalloproteinases and their inhibitors in patients with Kawasaki disease.

BACKGROUND: Accelerated matrix breakdown caused by the increased activity of matrix metalloproteinases (MMPs) and/or the quantitative imbalance between MMP and tissue inhibitor of MMP (TIMP) have been implicated in several pathological conditions. MMP and TIMP may also be involved in the destruction of the coronary arterial wall and the resultant coronary arterial lesions in Kawasaki disease. METHODS AND RESULTS: Plasma levels of MMPs, neutrophil elastase, and TIMPs were measured by enzyme-linked immunoassay in 57 patients with Kawasaki disease and no coronary arterial lesions (group 1) and in 8 patients with Kawasaki disease and coronary arterial lesions (group 2). Blood samples were obtained before and after intravenous gamma globulin therapy and in the convalescent stage. Levels of MMPs, neutrophil elastase, and TIMPs were significantly higher in Kawasaki disease patients before gamma globulin therapy than in 18 age-matched afebrile control subjects and 17 age-matched febrile disease control subjects (P<0.01). More importantly, the pre-gamma globulin MMP9 level and MMP9/TIMP2 ratio and post-gamma globulin MMP3 level and MMP3/TIMP1 ratio were significantly higher in group 2 than in group 1 patients (P<0.05). Although MMP levels in febrile disease controls were significantly higher than those of afebrile controls, the MMP/TIMP ratios of febrile disease controls and afebrile controls were comparable. CONCLUSIONS: These data suggest that patients with Kawasaki disease and high levels of MMP and/or MMP/TIMP are susceptible to coronary arterial lesions. Studies of the effects of MMP inhibitors on coronary outcome may provide evidence that MMP is a viable therapeutic target for the prevention of coronary arterial lesions due to Kawasaki disease.

Child, Preschool↗
PubMed2001

The influences of molar intrusion on the inferior alveolar neurovascular bundle and root using the skeletal anchorage system in dogs.

The skeletal anchorage system (SAS) was developed as intraoral rigid anchors for open-bite correction by intrusion of molars. Since the application of SAS is a new modality in orthodontic treatment, the influences of radical molar intrusion on the root and the inferior alveolar neurovascular bundle were unknown. The purpose of this research is to verify the effect of molar intrusion on the neurovascular bundle, the level of osseointegration of bone screws, and root resorption. The results of this study showed mandibular molars were intruded 3.4 mm on the average over 7 months in dogs. The miniplates were well stabilized with osseointegrated bone screws and the peri-implant soft tissues showed slight inflammatory changes. Neither nerves nor blood vessels were damaged. Root resorption was observed but was repaired with new cementum. We concluded that the SAS utilizing transmucosal titanium miniplates as an immovable orthodontic anchorage could provide a new modality for molar intrusions without serious iatrogenic problems.

Alveolar Process↗
PubMed2000

Effects of ketamine on formalin-induced activity in the spinal dorsal horn of spinal cord-transected cats: differences in response to intravenous ketamine administered before and after formalin.

BACKGROUND: Although formalin has been widely used as an algesic substance in rodent studies, the unique biphasic effect seen in rats is not present in humans. Humans, like cats, have a monophasic behavioral response to formalin injection. Electrophysiologically, spinal dorsal horn neurons in cats also have what could be considered a monophasic response after the initial burst of activity following formalin injection. Although several studies of the effects of ketamine on formalin responses have been carried out in rodents, we are unaware of similar studies in cats. We hypothesize that such species differences may explain observed differences in preemptive analgesic effects. Therefore, we examined the effects of ketamine on activity of spinal wide dynamic range (WDR) neurons evoked by formalin injection in cats. METHODS: We investigated in cats the effect of ketamine on the activity of WDR neurons in the spinal dorsal horn that was evoked by formalin. In addition, we studied the effects of pre- and post-administration of ketamine on the maintained phase of the formalin response. Each dose was a subanesthetic, anesthetic or high anesthetic dose (3.0 mg x kg(-1), 10 mg x kg(-1), and 30 mg x kg(-1)). RESULTS: Intravenously administered ketamine produced a dose-dependent depression of evoked activity that was significantly greater when the drug was administered before formalin. CONCLUSION: In spite of the species differences in responses to formalin, there still appears to be a clear preemptive effect of ketamine in the cat. Species differences may not explain apparent differences between human and animal preemptive analgesia.

Anesthetics, Dissociative↗
PubMed2000

[The anesthetic management for elective or emergent cesarean section in patients with intracranial arteriovenous malformation].

Subarachnoid hemorrhage secondary to ruptured intracranial arteriovenous malformation (AVM) during pregnancy, although rare, is a grave complication. We experienced 3 patients with AVM for cesarean section. Case 1: A 24-year-old woman suffered sudden vomiting and headache during the 22nd week of her first pregnancy. She was diagnosed as having the intracranial hemorrhage due to AVM. Because the patient was bleeding again at 29th week of pregnancy, emergency operation was performed. Her neurological symptom improved. Cesarean section was performed under general anesthesia at 34th week of pregnancy. Case 2: A 42-year-old woman of her first pregnancy had past history of subarachnoid hemorrhage due to AVM at the ages of 23, 28, 29 and 36. The malformation was not corrected surgically. Her neurological status was normal. Cesarean section was performed under spinal anesthesia. Case 3: A 29-year-old woman suffered sudden hemiplegia, vomiting and headache during the 40th week of her first pregnancy. She was diagnosed as having intracranial hemorrhage. Cesarean section immediately followed by the removal of an intra cranial hematoma under general anesthesia. Better perinatal outcome is expected when AVM rerupture is prevented by first performing cesarean section.

Adult↗
PubMed1999

Skeletal anchorage system for open-bite correction.

A skeletal anchorage system was developed for tooth movements. It consists of a titanium miniplate that is temporarily implanted in the maxilla or the mandible as an immobile anchorage. In this article, we introduce the skeletal anchorage system to intrude the lower molars in open-bite malocclusion and evaluate the results of treatment in two severe open-bite cases that underwent orthodontic treatment with the system. Titanium miniplates were fixed at the buccal cortical bone around the apical regions of the lower first and second molars on both the right and left sides. Elastic threads were used as a source of orthodontic force to reduce excessive molar height. The lower molars were intruded about 3 to 5 mm, and open-bite was significantly improved with little if any extrusion of the lower incisors. No serious side-effects were observed during the orthodontic treatment. The system was also very effective for controlling the cant and level of the occlusal plane during orthodontic open-bite correction.

Adolescent↗
PubMed1999

Loperamide (ADL 2-1294), an opioid antihyperalgesic agent with peripheral selectivity.

The antihyperalgesic properties of the opiate antidiarrheal agent loperamide (ADL 2-1294) were investigated in a variety of inflammatory pain models in rodents. Loperamide exhibited potent affinity and selectivity for the cloned micro (Ki = 3 nM) compared with the delta (Ki = 48 nM) and kappa (Ki = 1156 nM) human opioid receptors. Loperamide potently stimulated [35S]guanosine-5'-O-(3-thio)triphosphate binding (EC50 = 56 nM), and inhibited forskolin-stimulated cAMP accumulation (IC50 = 25 nM) in Chinese hamster ovary cells transfected with the human mu opioid receptor. The injection of 0.3 mg of loperamide into the intra-articular space of the inflamed rat knee joint resulted in potent antinociception to knee compression that was antagonized by naloxone, whereas injection into the contralateral knee joint or via the i.m. route failed to inhibit compression-induced changes in blood pressure. Loperamide potently inhibited late-phase formalin-induced flinching after intrapaw injection (A50 = 6 microgram) but was ineffective against early-phase flinching or after injection into the paw contralateral to the formalin-treated paw. Local injection of loperamide also produced antinociception against Freund's adjuvant- (ED50 = 21 microgram) or tape stripping- (ED50 = 71 microgram) induced hyperalgesia as demonstrated by increased paw pressure thresholds in the inflamed paw. In all animal models examined, the potency of loperamide after local administration was comparable to or better than that of morphine. Loperamide has potential therapeutic use as a peripherally selective opiate antihyperalgesic agent that lacks many of the side effects generally associated with administration of centrally acting opiates.

Analgesics, Opioid↗
PubMed1998

X-inactivation pattern in the liver of a manifesting female with ornithine transcarbamylase (OTC) deficiency.

Ornithine transcarbamylase (OTC) deficiency is the most common urea cycle disorder. It is X-linked and hemizygous new-born males usually suffer fatal hyperammonemia. In contrast, carrier females manifest variable phenotypes, ranging from asymptomatic carriers to those with severe hyperammonemia. In order to understand the correlation between X-inactivation status and the clinical phenotype of carrier females with this disorder, we analyzed the X-inactivation pattern of peripheral blood leukocytes in a family consisting of a clinically normal mother and two daughters with severe manifestation. In addition, we obtained tissue samples from various parts of the liver of one of these daughters and analyzed X-inactivation patterns and the residual OTC activities. The X-inactivation of peripheral blood leukocytes was nearly random in these carrier females and showed no correlation with the disease phenotype. However, the X-inactivation of the liver was much more skewed and correlated well with the OTC activity of all samples. Interestingly, the degree of X-inactivation varied considerably, even within the same liver.

Child↗
PubMed1998

[The effects of sevoflurane, isoflurane or enflurane on the pattern of phrenic nerve discharge in rabbits].

In order to estimate primary action of anesthetic agents on the central neural mechanisms of respiratory control and the ventilatory response to an acute increased ETCO2, the effect of sevoflurane (SEV), isoflurane (ISO) or enflurane (ENF) on the pattern of phrenic nerve discharge (Phr.N.A.) was studied in adult rabbits which had been vagotomized, paralyzed and ventilated artificially with 100% oxygen. Throughout the course of experiment, ETCO2 and the rectal temperature of animals were maintained around physiological values. Depressant effects of these anesthetics on Phr. N.A. which consisted of inspiratory slope (SLO), peak amplitude (AMP), inspiratory (Ti) and expiratory (Te) time, I/E ratio (I/E) and respiratory cycle (Tc) were evaluated and compared with each anesthetic. At 0.5 MAC administration, SEV and ISO reduced SLO and AMP without a remarkable change in Tc, but ENF did with a prolongation in Tc. Inhalation of each anesthetic with 1 MAC caused a marked respiratory slowing with a more reduction of SLO and AMP than those occurred at 0.5 MAC; SEV increased Te more than Ti, but ENF prolonged Ti more than Te, while ISO enhanced both Ti and Te without any change of I/E. An acutely increased ETCO2 after the respiratory arrest (RA test) induced the change of Phr.N.A which was characterized by a marked prolongation in Tc with a prolonged Te, an increased SLO and an augmented AMP. The prolonged Tc induced by RA test was diminished by the inhalation of anesthetics, and a new response, shortening in Ti was produced by ENF and ISO. Based on these results, it might be concluded that there are both quantitative and qualitative differences in these anesthetic effects on the central pattern generator of respiration and the mechanism of CO2 responses at equipotent anesthetic concentrations.

Action Potentials↗
PubMed1997

Effects of triamcinolone on brain and cerebrospinal fluid apolipoprotein E levels in rats.

The effects of the short term administration of triamcinolone (0.5 mg per 100 g body weight, 5 days) on apolipoprotein E and A-I concentrations in cerebrospinal fluid (CSF), brain extract and serum were studied in male Wistar rats using enzyme immunoassays. ApoE was significantly increased by triamcinolone in apoE-rich HDL1 in serum; 40+/-13 (mean+/-SD) vs. 68+/-23 mg/dl (15 saline-treated rats vs. 11 triamcinolone-treated rats)(P<0.01), which was paralleled by an increase in serum apoA-I (76+/-21 vs. 184+/-24 mg/dl), while serum lipids also increased significantly. No significant difference was observed in the apoE concentrations in CSF (296+/-170 vs. 269+/-67 microg/dl) or brain extract (5.0+/-1.6 vs. 5.7+/-1.8 microg/g wet weight). The apoA-I concentrations found in CSF and brain extract were much lower than those for apoE and were not appreciably affected by triamcinolone: 7.7+/-5.5 vs. 4.5+/-3.1 microg/dl for CSF and <0.5 vs. <0.5 microg/g wet weight for brain extract. The apo E metabolism in the rat central nervous system appears to be refractory to the short term administration of triamcinolone and to changes in the serum lipoprotein metabolism. ApoA-I appears unlikely to play a significant role in the rat central nervous system.

Animals↗
PubMed1997

The natural course of anterior disc displacement without reduction in the temporomandibular joint: follow-up at 6, 12, and 18 months.

PURPOSE: The purpose of this study was to examine the natural course of anterior disc displacement without reduction in the temporomandibular joint (TMJ). PATIENTS AND METHODS: The subjects were patients who had been diagnosed as having anterior disc displacement without reduction in the TMJ, but who had not undergone any treatment. Forty-four patients were followed for 6 months, 38 for 12 months, and 22 for 18 months. Clinical signs and symptoms were evaluated at each follow-up, and the incidence of successful resolution was determined using the criteria established in 1984 by the American Association of Oral and Maxillofacial Surgeons. RESULTS: The range of motion increased at each time during the follow-up period. Tenderness in the TMJ and the masticatory muscles was alleviated, but the noise in the TMJ remained unchanged at each follow-up time. The incidence of successful resolution was 34.1% at 6 months, 50.0% at 12 months, and 68.2% at 18 months. CONCLUSIONS: The clinical signs and symptoms of anterior disc displacement without reduction tend to be alleviated during the natural course of the condition. This should be taken into consideration when anterior disc displacement without reduction is treated.

Adolescent↗
PubMed1997

[Effect of nitrous oxide on spinal dorsal horn WDR neuronal activity in cats].

The effects of nitrous oxide (75%) on the spinal dorsal born wide dynamic range (WDR) neuronal activity were studied in either spinal cord intact or spinal cord-transected cats. Extracellular activity was recorded in the dorsal horn from single WDR neurons responding to noxious and non-noxious stimuli applied to the cutaneous receptive fields on the left bind foot pads of intact or decerebrate, spinal cord-transected (L 1-2) cats. The experiment was divided into four sections as follows: (1) When 10 micrograms of bradykinin (BK) was injected into the femoral artery ipsilateral to the recording site as the noxious test stimulus in the spinal cord-transected cat, all of 6 WDR neurons gave excitatory responses which were not depressed by 75% nitrous oxide. (2) When the injection of 10 micrograms of BK into the femoral artery ipsilateral to the recording site was used in the spinal cord-intact cat, 6 of 15 WDR neurons (40%) gave excitatory responses, which were significantly depressed by 75% nitrous oxide, and 9 of 15 WDR neurons (60%) gave inhibitory responses, which were not affected by 75% nitrous oxide. (3) When 10 micrograms of bradykinin (BK) was injected into the femoral artery contralateral to the recording site as the noxious test stimulus in the spinal cord transected cat, 6 of 12 WDR neurons gave excitatory reasons, which were not depressed by 75% nitrous oxide. (4) When the injection of 10 micrograms of BK into the femoral artery contralateral to the recording site was used in the spinal cord-intact cat, 6 of 6 WDR neurons (100%) gave responses, which were affected by 75% nitrous oxide. We have observed that nitrous oxide reduces the excitation and inhibition of dorsal born WDR neuronal activities induced by BK injection in spinal cord-intact cats, but does not reduce the excitation of those in spinal cord-transected cats. This finding confirmed that the antinociceptive effect of nitrous oxide might be modulated by supraspinal descending inhibitory control systems. In addition our result showed that the supraspinal effect of nitrous oxide was mediated not only by an increase but also a decrease in a supraspinal descending inhibition.

Action Potentials↗
PubMed1997

[The effects of isoflurane on the formalin-induced activity in the spinal dorsal horn of transected cat].

Although the formalin test is widely used in rodents, the electrical response to this stimulus and the effect of isoflurane on this response, has not been well understood in cats. We have therefore examined the effect of isoflurane on spinal wide-dynamic-range neuronal activity evoked by a subcutaneous (s.c.) formalin injection in cats. In decerebrate, spinal cord-transected cats (L 1-2), a s.c. injection of formaldehyde solution (0.05 ml; 5%) was performed in the receptive fields of spinal wide-dynamic-range neurons at the hind paw. Isoflurane (1.5%) inhalation was given 20 mins prior to formalin injection or 5 mins after the formalin injection. The formalin injection elicited an immediate and continuous discharge or burst activity in the neurons that lasted at least 90 min. Inhaled isoflurane was found to markedly inhibit this neuronal discharge. At 30 mins after discontinuing of isoflurane, the neuronal activity in both groups recovered to approximately 55% of the control value. These results suggest that formalin injection will reliably produce a continuous burst of neuronal activity in the spinal dorsal horn of cats, and that this activity can be markedly reduced by isoflurane. The ability of isoflurane to inhibit this neuronal response was not temporally related to the formalin injection.

Administration, Inhalation↗
PubMed1996

Native lipoproteins inhibit platelet activation induced by oxidized lipoproteins.

Copper-catalyzed oxidation of low-density lipoproteins (LDL) (0.8 g protein/l LDL, 20 mumol/l CuSo4, 37 degrees C) resulted in the formation of thiobarbituric reactive substances that was substantially completed at 24 hrs whereas their formation from high-density lipoproteins (HDL) plateaued at only 25% of that amount after 8 hrs. The oxidized lipoproteins induced aggregation and increases in [Ca2+]i in washed platelets, but not in platelet-rich plasma, and these activating effects were not inhibited by aspirin or EGTA but were inhibited by both of the native lipoproteins. These results show that oxidized HDL, like oxidized LDL, have platelet activating ability and suggest that the native lipoproteins may play a crucial role in preventing the oxidized lipoprotein-mediated platelet activation.

Aspirin↗
PubMed1996

Peripheral and spinal actions of opioids in the blockade of the autonomic response evoked by compression of the inflamed knee joint.

BACKGROUND: Three types of opioid receptors, mu, delta, and kappa, are present in the periphery and in the central nervous system. In contrast to the effects in the central nervous system, the antinociceptive action of opioids in the periphery is not as well characterized. The effects of intraarticular, spinal, and intramuscular injections of mu, delta, and kappa opioid agonists on the autonomic response evoked by compression of an inflamed knee joint were evaluated. METHODS: In halothane-anesthetized rats, arthritis was induced by injecting kaolin and carrageenan into the right knee joint. Standardized compression of the knee joint by inflation of a pediatric blood pressure cuff to 200 mmHg for 2 min produced a reliable stimulus-dependent hypertension (delta = 13 mmHg). Drugs were delivered intramuscularly, intrathecally through a chronic catheter, or intraarticularly into the right knee joint. The drug injection was performed 4 hr after induction of the inflammation. RESULTS: The intrathecal administration of mu, delta, and kappa agonists resulted in a dose-dependent blockade of the cuff-evoked increase in blood pressure. The order of intrathecal drug activity on the compression-evoked blood pressure responses with median effective dose (ED50) was sufentanil (0.02 nmol; mu) > PD117302 (0.5 nmol; kappa); spiradoline (1.5 nmol; kappa) morphine (2.4 nmol; mu) > DADL (15 nmol; delta); DPDPE (18 nmol; delta) > U-50,488H (620 nmol; kappa) > naloxone = 0. The intraarticular administration of mu and kappa, but not delta agonists, produced a dose-dependent blockade of a compression-evoked increase in blood pressure, with the order of drug activity (ED40) as follows: sufentanil (0.04 mumol) > PD117302 (0.3 mumol); spiradoline (0.8 mumol), morphine (0.9 mumol) > U-50,488H (0.9 mumol) > DPDPE (> 5 mumol); DADL (> 18 mumol) > naloxone = 0. Intramuscular injection of these agonists caused suppression, with the order of drug activity (ED50) as follows: sufentanil (0.2 mumol) > PD117302 (2 mumol); spiradoline (11 mumol) morphine (9 mumol) > DPDPE (> 5 mumol); DADL (18 mumol) > U-50,488H (22 mumol) > naloxone = 0. All intraarticular effects were reversible by injecting naloxone intramuscularly, with the ordering of naloxone potency against equiactive doses of morphine > U50,488H. CONCLUSIONS: The activity of the respective agonists and the intraarticular > intramuscular ordering of systemic potency in this model indicate that opioids, by an action at mu and kappa, can exert a direct antihyperalgesic action at the terminals of primary afferents projecting to a region of inflammation. These observations offer strong support for a peripheral action of opioids in certain states in inflammation-induced hyperalgesia.

Analgesia↗