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Biomedical subjects

T Sakamoto

Publications and source records attributed to T Sakamoto.

At least 703 records · Page 39Linked to original sources

Capsaicin applied to rat lumbar intervertebral disc causes extravasation in the groin skin: a possible mechanism of referred pain of the intervertebral disc.

Administration of 10 micrograms of capsaicin into the anterior portion of a lumbar intervertebral disc of rats pretreated with Evans blue (i.v.) caused dye extravasation in the groin skin. This phenomenon occurred even when the spinal nerve of the same segment, bilateral sympathetic trunks, and/or the anterior L2 spinal root had been cut; it did not occur in rats with a cut genitofemoral nerve. Infiltration of capsaicin solution directly into the genitofemoral nerve did not cause dye extravasation. These results suggested the presence of dichotomizing sensory C-fibers which innervate both the intervertebral discs and the groin skin in the L2 spinal nerve. If such dichotomizing fibers exist in man, they may contribute to the groin pain sometimes associated with intervertebral disc lesions.

Animals↗

Difference in plasminogen activator inhibitor activity between non-Q-wave infarction and Q-wave infarction.

We examined the plasma levels of tissue plasminogen activator antigen and plasminogen activator inhibitor activity in 14 patients with non-Q-wave infarction and in 27 patients with Q-wave infarction before the start of thrombolytic therapy and in 34 control subjects. The mean level of plasma tissue plasminogen activator antigen (ng/ml) was higher (P < 0.01) both in the patients with non-Q-wave infarction and in those with Q-wave infarction than in the control subjects (10.3 +/- 1.9, 9.5 +/- 0.8 vs. 5.8 +/- 0.3), and there was no difference in the level between the patients with non-Q-wave infarction and those with Q-wave infarction. The mean level of plasma plasminogen activator inhibitor activity (IU/ml) was lower (P < 0.01) in the patients with non-Q-wave infarction than in those with Q-wave infarction (7.3 +/- 2.0 vs. 17.1 +/- 2.2), and there was no difference in the level between the patients with non-Q-wave infarction and the control subjects (7.3 +/- 2.0 vs. 4.1 +/- 2.6). The patency rate of infarct-related coronary artery before thrombolytic therapy was higher (P < 0.01) in the patients with non-Q-wave infarction than in those with Q-wave infarction (54% vs. 15%). We conclude that plasminogen activator inhibitor activity was lower in non-Q-wave infarction than in Q-wave infarction and this may be related to the higher patency rate of infarct-related coronary artery in non-Q-wave infarction.

Aged↗

Effects of tracheostomy on electrically induced vocalization in decerebrate cats.

Electrical stimulation delivered to the rostral pons induced well coordinated activity of the intralaryngeal muscles and the ventilatory muscles for vocalization in unanesthetized, decerebrate cats. The stimulation reset the normal respiratory rhythm and induced vocalization with a newly developed rhythm. Continuous opening of the tracheostomy decreased the breathing cycle during induced vocalization. Opening of the prepared tracheostomy during vocalization caused a sudden decrease in the subglottic pressure, but the expiration phase was not abruptly terminated. These findings suggested that vagal feedback from pulmonary stretch receptors plays a more significant role in the maintenance of the breathing cycle during electrically induced vocalization than the laryngeal feedback from the laryngeal mucosa.

Animals↗

Expression of insulin-like growth factor I gene in osmoregulatory organs during seawater adaptation of the salmonid fish: possible mode of osmoregulatory action of growth hormone.

Growth hormone has been shown to contribute to seawater adaptation of salmonid fishes. The growth influence of growth hormone is mediated largely by hepatic production of insulin-like growth factor I (IGF-I). To study the growth hormone-IGF-I axis in osmoregulation, we measured IGF-I mRNA in the liver, gill, and body kidney from rainbow trout by Northern analysis. The levels of IGF-I mRNA in all tissues increased significantly after injection of growth hormone. Transfer of trout from fresh water to 80% seawater evoked an increase in plasma growth hormone after 1 day. IGF-I mRNA was not altered significantly in the liver, but it was increased in the gill and body kidney after 1 and 8 days, respectively. These observations indicate that the IGF-I gene is expressed differently among these organs during seawater adaptation. Growth hormone may stimulate hypoosmoregulatory ability by inducing local expression of IGF-I in osmoregulatory organs, although the possibility that IGF-I expression might occur in part independently of growth hormone during seawater adaptation cannot be excluded.

Animals↗

Antimicrobial activity of lipoprotein particles containing apolipoprotein Al.

Human plasma in vitro inhibits the growth of coagulase negative staphylococci, S. epidermidis, which may be pathogenic in the immunocompromised host. To determine the antimicrobial components, serum was fractionated by column chromatography, which revealed that elution areas where lipoproteins can be yielded had high antimicrobial activity against S. epidermidis. Therefore, lipoprotein fractions, including very low density lipoprotein (VLDL), low density lipoprotein (LDL) and high density lipoprotein (HDL), were separated by ultracentrifugation and incubated with S. epidermidis. All 3 lipoprotein fractions suppressed bacterial growth within the first 3 h but VLDL enhanced bacterial growth after 9 h of incubation compared with the control. HDL, however, inhibited bacterial growth throughout 21 h of incubation. To confirm these results, serum from healthy volunteers was separated by ion exchange column chromatography and again by HPLC to purify the antimicrobial fraction. In the protein analysis with gradient polyacrylamide-SDS gel, apolipoprotein Al (apo Al), which is a major apolipoprotein of HDL, was detected in the antimicrobial fraction. Therefore, this fraction was loaded onto an immunoaffinity column coupled with the anti-apo Al monoclonal antibody (Mab). Unbound fraction had no antimicrobial activity, but anti-S. epidermidis activity was recovered from the bound fraction which consisted mainly of apo Al, All and apo C in protein composition. These results indicated that the antimicrobial activity was associated with the apo Al-containing lipoprotein particles (HDL). This property of HDL may directly affect bacterial growth and promote the self-defense mechanisms of normal and immunocompromised individuals.

Anti-Bacterial Agents↗

Effect of CP-96,345, a non-peptide NK1 receptor antagonist, against substance P-, bradykinin- and allergen-induced airway microvascular leakage and bronchoconstriction in the guinea pig.

We have investigated the effect of a new non-peptide NK1 receptor antagonist, CP-96,345, against substance P (SP)-, bradykinin (BK)- and allergen-induced airway microvascular leakage, bronchoconstriction and hypotension in anesthetized guinea pigs. Lung resistance (RL) and mean systemic blood pressure (BP) were measured for 6 min after challenge, followed by measurement of extravasation of Evans blue dye into airway tissues, used as an index of airway microvascular leakage. I.v. (2 nmol/kg) and inhaled (1 mM, 45 breaths) SP, i.v. (15 nmol/kg) and inhaled (1 mM, 45 breaths) BK and aerosolized allergen (5 mg/ml of ovalbumin, 30 breaths) induced a significant increase in RL and leakage of dye at all airway levels, and decreased BP significantly except for inhaled BK. CP-96,345 (2 mg/kg i.v.) abolished the dye extravasation induced by both SP. CP-96,345 partly inhibited the responses induced by both BK but not by allergen. CP-96,345 markedly inhibited the increase in RL and fall in BP induced by SP but not by BK or allergen. NK1 receptor-mediated mechanisms may contribute to SP- and BK-induced airway microvascular leakage and SP-induced bronchoconstriction and hypotension. These mechanisms are not important in the acute airway responses induced by inhaled allergen.

Administration, Inhalation↗

Intercellular adhesion molecule-1 on rat corneal endothelium in experimental uveitis.

We studied the expression of the intercellular adhesion molecule-1 (ICAM-1) on the corneal endothelium of the rat in the experimental uveitis induced by interphotoreceptor peptides (R-4) as an immunogen using immunohistochemical methods. ICAM-1, which was not detected in eyes without inflammation, was expressed on the corneal endothelium, vascular endothelium and inflammatory cells, such as monocytes and lymphocytes, in R-4 induced uveitis. The ocular inflammation in the iris, ciliary body and anterior chamber associated with the adherence of inflammatory cells to the corneal endothelium (keratic precipitates) first appeared on the 11th day and were most remarkable on the 14th day and then gradually subsided after 18th day. The expression of ICAM-1 on the corneal endothelium was noticed from the 12th day of immunization to the 16th day and was most prominent on the 14th day but disappeared after the 18th day. The present study proved that ICAM-1 was expressed on the corneal endothelium in anterior uveitis and further indicated that the corneal endothelium modulates the inflammation of the anterior ocular segment by expressing ICAM-1 and forming keratic precipitates.

Animals↗

The human prohibitin (PHB) gene family and its somatic mutations in human tumors.

Five cosmid clones, isolated by procedures to screen genomic libraries for homologous variants of the human prohibitin gene (PHB), were analyzed to determine their genomic structures. Four of these (PHBP1-4) were found to be processed pseudogenes, each located on a different chromosome from their counterparts on chromosome 17q21. The DNA sequence of one clone (PHBP1, on chromosome 6q25) shared a 91.3% identity at the nucleotide level with the cDNA of functional prohibitin. A large number of human tumors of the breast, ovary, liver, and lung were examined for somatic mutations in the PHB gene. Although mutations were observed in a few sporadic breast cancers, none were identified in any of the other cancers.

Base Sequence↗

Structure of a cyanobacterial gene encoding the 50S ribosomal protein L9.

The rplI gene encoding the ribosomal protein L9 was found 4 kbp downstream from the desA gene, but on the opposite strand, in the genome of the cyanobacterium Synechocystis PCC6803. The deduced amino acid sequence is homologous to the sequences of the L9 proteins from Escherichia coli and chloroplasts of Arabidopsis and pea. The gene is present as a single copy in the chromosome and is transcribed as a mRNA of 0.64 kb. An open reading frame of unknown function (ORF291) was found in the upstream region of the rplI gene.

Amino Acid Sequence↗

Immunohistochemical localization of superoxide dismutase in congenital hydrocephalic rat brain.

The effects of active oxygen species in the development of congenital hydrocephalus have been investigated. Superoxide dismutase (SOD) is one of the scavengers of active oxygen species and there have been many recent reports on the relationship between neurological disorders by active oxygen species following reperfusion for ischemic brain and SOD. In this study, the localization of Cu-SOD and Zn-SOD in WIC-Hyd congenitally hydrocephalic rat brains was identified by the enzyme unlabeled antibody method. We examined the localization of SOD in the choroid plexus, hippocampus, and ependymal cells of the lateral ventricle and aqueduct of WIC-Hyd rats. SOD was hardly observed in the choroid plexus and faintly localized in the hippocampus and ependymal cells of the congenitally hydrocephalic brain, but was observed equally in the cytoplasm of the choroid plexus, hippocampus, and ependymal cells in control animals. In the hippocampus, less SOD was found in hydrocephalic rats than in controls. The SOD was slightly observed in the CA1 pyramidal cells in hydrocephalic rats. In the lateral ventricle and aqueductal ependyma, less SOD was found in hydrocephalic than in controls rats. The amount of Cu, Zn-SOD in the congenitally hydrocephalic rat brain was less than in the control, especially in the choroid plexus. Therefore, we suspect that the production of SOD is congenitally reduced in the congenitally hydrocephalic rat brain, and this may promote the impairment of the function of choroid plexus and cilia due to increased active oxygen species. The reduction of SOD in the choroid plexus, hippocampus and ependymal cells of ventricles or aqueduct may promote the development of hydrocephalus in the congenitally hydrocephalic rat.

Animals↗

Subarachnoid fluid collection in infants complicated by subdural hematoma.

In the natural history of infantile extracerebral fluid collections, subarachnoid fluid collection itself is regarded as a benign lesion, and surgical treatment is not indicated. As this condition is age-related and self-limiting, spontaneous resolution can be expected in most cases by 2-3 years of age. However, out of 20 cases of infantile subarachnoid fluid collection in an 8-year period, 3 infants developed subdural hematoma. Infantile subarachnoid fluid collection seems to be prone to complicate subdural hematoma. Surgical treatment should be considered when subarachnoid fluid collection is complicated by subdural hematoma due to arachnoid ruptures or tearing of the bridging veins. Therefore, all patients should be observed closely and measures should be taken to prevent head trauma since it may precipitate subdural hematoma.

Diagnosis, Differential↗

Effect of beta 2-adrenoceptor agonists against platelet-activating factor-induced airway microvascular leakage and bronchoconstriction in the guinea pig.

We have investigated the effect of inhaled formoterol (0.75 mg/ml, 60 breaths) and salbutamol (25 mg/ml, 60 breaths) against airway microvascular leakage and bronchoconstriction induced by inhaled platelet-activating factor (PAF) and histamine in anaesthetized guinea pigs. Lung resistance (RL) was measured for 6 min after challenge, followed by measurement of extravasation of Evans blue dye into airway tissues, used as an index of airway microvascular leakage. PAF (0.1, 0.4 and 1 mM; 30 breaths) caused a significant increase in RL and extravasation of dye, but the responses were smaller than those induced by histamine (5 mM, 30 breaths). Both formoterol and salbutamol caused a small but significant inhibition of extravasation in the distal intrapulmonary airways induced by PAF (0.1 and 0.4 mM for formoterol and 0.1 mM for salbutamol), and only formoterol reduced the increase in RL induced by 1 mM PAF. These drugs also inhibited both airway effects of histamine to a higher degree. In conclusion, formoterol and salbutamol can partly inhibit airway microvascular leakage and bronchoconstriction induced by inhaled PAF and histamine. The inhibitory potency of beta 2-adrenoceptor agonists may be dependent on the inflammatory mediator inducing the airway effects.

Administration, Inhalation↗

Role played by NK2 receptor and cyclooxygenase activation in bradykinin B2 receptor mediated-airway effects in guinea pigs.

We have investigated the effects of SR-48968, an NK2 receptor antagonist, and indomethacin, a cyclooxygenase inhibitor, against bronchoconstriction and airway microvascular leakage induced by bradykinin (BK) in anesthetized guinea pigs. In addition, we have determined whether these effects were mediated via bradykinin B2 receptor activation, using a B2 receptor antagonist HOE 140. Lung resistance (RL) and extravasation of Evans blue dye into airway tissues were used as indexes of airway caliber and microvascular leakage, respectively. BK (15 nmol/kg i.v.) induced a significant increase in RL and leakage of dye at all airway levels, responses which were completely abolished by HOE 140 (0.13 mg/kg i.v.). SR-48968 (1.5 mg/kg i.v.) had no effect against BK-induced airway effects. Indomethacin (5 mg/kg i.v.) completely blocked the increase in RL and significantly inhibited the leakage of dye in peripheral intrapulmonary airway. In conclusion, bronchoconstriction induced by i.v. BK is mediated by release of cyclooxygenase products but not by stimulation of NK2 receptors, while the airway microvascular leakage only partly involves cyclooxygenase activation. Cyclooxygenase activation may occur following bradykinin B2 receptor stimulation.

Airway Resistance↗

Autoimmunity during alpha-interferon therapy for chronic hepatitis C.

One hundred twenty-five patients with chronic hepatitis C were treated with natural IFN alpha or recombinant IFN alpha-2a, daily doses of 3 MU or 9 MU, respectively. IFNs were given 6 times a week for the first 2 weeks followed by thrice weekly administration for 12 weeks or more. ANA, TMA, AMA and anti-DNA antibody newly developed in 8, 1, 2 and 1 patient, respectively. Furthermore, we encountered some cases in which underlying autoimmune disorders were thought to be exacerbated by IFNs. It is important to pay sufficient attention to the development of autoimmune diseases in IFN therapy for chronic hepatitis C.

Adult↗

Elevated plasma interleukin-6 levels in patients with acute myocardial infarction.

Interleukin-6 (IL-6) plays a key role in the synthesis of human acute-phase protein and several acute-phase responses occur in patients with acute myocardial infarction (AMI). We examined the plasma levels of IL-6 in 23 consecutive patients with AMI over the course of 4 weeks and in 30 control subjects. In patients with AMI, the plasma IL-6 levels (in picograms per milliliter) were increased at all sampling points from admission to discharge (ranging from 28.5 +/- 6.6 to 46.5 +/- 7.8) compared with levels in control subjects (11.4 +/- 2.9; p < 0.01). Cardiac catheterization did not influence plasma IL-6 levels. The plasma IL-6 level reached its peak approximately 3 days (46.5 +/- 7.8) and approximately 1 week after admission in patients with AMI. There was a significant positive linear correlation between the peak level of plasma IL-6 minus the level on admission and the peak level of plasma C-reactive protein in patients with AMI. The peak IL-6 level did not correlate with the peak levels of creatine kinase, pulmonary capillary wedge pressure, or left ventricular ejection fraction at 4 weeks. We conclude that the plasma IL-6 level is increased over a time course of 4 weeks in patients with AMI.

Acute-Phase Reaction↗