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Biomedical subjects

S Kitahara

Publications and source records attributed to S Kitahara.

At least 19 recordsLinked to original sources
PubMed1995

Rapid identification of Streptococcus pneumoniae by PCR amplification of ribosomal DNA spacer region.

Streptococcus pneumoniae is one of the important human pathogens in clinical microbiology. A polymerase chain reaction assay was designed to detect and identify S. pneumoniae through amplification of the ribosomal DNA spacer regions between the pneumococcal 16S-23S ribosomal RNA genes. Thirty-two Streptococcus and non-Streptococcus strains were tested to verify the specificity of the assay, and only S. pneumoniae strains gave a positive reaction. This method is a powerful technique for the rapid identification of S. pneumoniae.

Bacteriological Techniques↗
PubMed1995

Exhibition of anti-platelet effect of isocarbacyclin methyl ester and its free acid via an increase in cAMP in platelets.

Isocarbacyclin methyl ester (CAS 88931-51-5, TEI-9090) and its free acid (CAS 88911-35-7, TEI-7165) are chemically stable analogues of prostaglandin (PG) I2. The cAMP increasing activities of TEI-9090 and TEI-7165 were investigated. TEI-9090, TEI-7165, PGI2, and PGE1 caused the accumulation of cAMP in rabbit and human platelets. The effects of TEI-9090, TEI-7165, and PGE1 were longer lasting than the effect of PGI2. Each drug concentration-dependently increased the cAMP level in rabbit and human platelets. The order of cAMP-increasing activity was PGI2 > PGE1 = TEI-9090 = TEI-7165 in rabbit platelets and PGI2 > TEI-9090 = TEI-7165 > PGE1 in human platelets. The antiplatelet aggregation activity of TEI-9090 in rabbit and human platelets was remarkably decreased by the addition of an esterase inhibitor, diisopropyl fluorophosphate (DFP). However, this activity of TEI-7165 was not affected by the inhibitor. In the presence of DFP, the cAMP accumulation by TEI-9090 in rabbit platelets was almost completely inhibited but that by TEI-7165 was not inhibited. These results suggest that TEI-9090 is deesterified to TEI-7165 and that this free acid then inhibits platelet aggregation via an increase in the cAMP level in the platelets.

Alprostadil↗
PubMed1995

Anti-platelet effects of isocarbacyclin methyl ester on human and rabbit platelets in vitro.

Anti-platelet effects of isocarbacyclin methyl ester (CAS 88931-51-5, TEI-9090) and of its free acid form, TEI-7165 (CAS 88911-35-7) were compared with those of prostaglandin (PG) I2 and PGE1. TEI-9090 and TEI-7165 dose-dependently inhibited human and rabbit platelet aggregation and human platelet adhesion in vitro. The IC50 values of TEI-9090, TEI-7165, PGI2, and PGE1 against ADP-induced human (rabbit) platelet aggregation were 22.90 (25.00) ng/ml, 2.78 (6.46) ng/ml, 1.67 (3.34) ng/ml, and 19.91 (8.32) ng/ml, respectively; and those against human platelet adhesion were 3.47 ng/ml, 0.13 ng/ml, 0.25 ng/ml, and 1.45 ng/ml, respectively. TTC-909, a product incorporating TEI-9090 in lipid microspheres, had an aggregation inhibitory effect similar to that of TEI-9090 in human platelets. The aggregation inhibitory effect of TEI-9090 and TTC-909 increased with incubation time, and reached a level similar to that of TEI-7165. In contrast, the aggregation inhibitory effect of TEI-7165 remained constant for 120 min, whereas that of PGI2 decreased with time. TEI-9090 and TEI-7165 also enhanced the disaggregation of human platelets at nearly the same concentration as they exerted their inhibitory effect on aggregation. The order of anti-platelet activities, compared at each optimum incubation point, were PGI2 approximately equal to TEI-7165 approximately equal to TEI-9090 (approximately equal to TTC-909) > PGE1 in human and rabbit platelets. These results indicate that TEI-9090 (TTC-909) and its active metabolite, TEI-7165, may be a potent anti-platelet drug.

Animals↗
PubMed1995

Ex vivo anti-platelet effects of isocarbacyclin methyl ester incorporated in lipid microspheres in rabbits.

Effect of TTC-909, a chemically stable isocarbacyclin methyl ester (CAS 88931-51-5, TEI-9090) incorporated in lipid microspheres, on platelet aggregation was tested in conscious rabbits. TTC-909 significantly inhibited platelet aggregation induced by ADP at early times after bolus i.v. injection from the dose of 0.3 micrograms/kg in a dose-dependent manner. Similarly, TTC-909 significantly inhibited platelet aggregation induced by ADP during the venous infusion from the dose of 100 ng/kg/min, also in a dose-dependent manner. The anti-platelet effect of TTC-909 was observed at a dose lower than that inducing hypotensive effect when given as both bolus i.v. and venous infusion. On the other hand, prostaglandin (PG) E1 (LM)--PGE1 incorporated in lipid microspheres--reduced blood pressure without having an anti-platelet effect. These results indicate that TTC-909 may be a potent anti-thrombotic drug.

Alprostadil↗
PubMed1995

[Sphingolipid changes in rat cerebral cortex during focal ischemia--how does ceramide accumulate in an ischemic condition?].

Levels of ceramide, sphingomyelin, cerebroside and gangliosides were determined in rat cerebral cortex during focal ischemia produced by middle cerebral artery occlusion. Ceramide began to increase at 6 hours of ischemia and increased to 4.5 folds at 96 hours. Amino-linked fatty acids in increased ceramide were composed solely of non-hydroxy fatty acids, and stearic acid was the most prominent. Sphingomyelin, whose amino-linked fatty acids were mostly stearic acid, decreased in a time-dependent manner and became about a half of controls at 96 hours. Hydroxy fatty acid linked cerebroside decreased at and after 6 hours of ischemia, whereas significant decrease of non-hydroxy fatty acid linked cerebroside occurred only at 96 hours of ischemia. There were no measurable changes in the levels of gangliosides. The results suggested that ceramide was produced in the cerebral cortex by the breakdown of sphingomyelin during ischemia.

Animals↗
PubMed1994

Effect of granulocyte colony-stimulating factor on neutropenia in liver transplant recipients with hypersplenism.

The authors present details of their initial experience with use of recombinant human granulocyte colony-stimulating factor (rhG-CSF) for preventing neutropenia caused by hypersplenism, and, possibly, for reducing the risk of postoperative infections in pediatric liver transplant recipients. Seven patients with end-stage liver disease, three of whom had severe hypersplenism, underwent living related liver transplantation (LRLT). The rhG-CSF was administered to the latter three patients. Peripheral neutrophil counts decreased immediately after reperfusion (to 1500 +/- 300/microL) in the three patients, and returned to normal with use of rhG-CSF 3 to 10 days after transplantation. The dosage was adjusted to maintain peripheral leukocyte and granulocyte counts above 5,000/microL and 2,000/microL, respectively. This initial clinical trial showed that rhG-CSF administration restores the leukocyte counts of patients who have hypersplenism, without any significant adverse effects, and that rhG-CSF holds promise for reducing the risk of infections after liver transplantation.

Child↗
PubMed1992

Is injectable collagen truly safe?

Most patients have no response to injectable collagen or silicone, but some cases may have positive or 'undersea' (= clinically negative but immunologically positive) response to collagen. From the results of the Macrophage migration inhibition test, the relative immunogenicity was augmented most when we used implants with the following combination. The first immunization was collagen and the second one was collagen with silicone. The augmented antigenicity might be enough to cause an allergic reaction to the patients who had no response to each implant alone.

Adjuvants, Immunologic↗
PubMed1992

The effects of gamma-glutamylcysteine ethyl ester, a prodrug of glutathione, on ischemia-reperfusion-induced liver injury in rats.

This study was designed to clarify the effects of changes in liver tissue glutathione (GSH) concentration on postischemic liver injury together with the effects of gamma-glutamylcysteine ethyl ester (GCE), a prodrug of GSH, and GSH. Rats were pretreated with GSH (50 mg/kg, i.v.), or GCE (50 mg/kg, i.v.), or untreated. In each rat, liver was isolated, and liver mitochondria were prepared after 2 h of ischemia or 1 h of reperfusion following 2 h of ischemia. Mitochondrial function was measured polarographically. Liver adenine nucleotide concentrations were also determined using high-performance liquid chromatography. Liver tissue GSH, an oxidized form of glutathione (GSSG) concentrations, and activities of GSH peroxidase and GSSG reductase were determined enzymatically. Liver hypoxanthine and xanthine concentrations were determined by HPLC. Liver tissue concentration of lipid peroxide was measured. Leakages of aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and adenine nucleotides into the hepatic vein after reperfusion were also measured. Administration of GCE improved the recovery of mitochondrial function and maintained tissue GSH concentration concomitantly. Increases in liver lipid peroxide concentration after reperfusion, and leakage of liver cell enzymes and adenine nucleotides were mitigated by administration of GCE. Administration of GSH itself failed to maintain tissue GSH concentration and had no protective effects. From these results, it is concluded that in the postischemic process, free radical formation might be enhanced, and the radical scavenging system deteriorated. To enhance the radical scavenging system is a possible maneuver to prevent radical-related cell damage associated with reperfusion, because pharmacological reduction of breakdown of ATP to hypoxanthine and xanthine seems to be difficult. GCE maintained liver GSH concentrations and mitigated postischemic liver injury, concomitantly. Clinical use of GCE might be recommended.

Adenine Nucleotides↗
PubMed1992

Effects of testosterone on gonadotropin subunit messenger ribonucleic acids in the presence or absence of gonadotropin-releasing hormone.

There is accumulating evidence that the negative feedback actions of testosterone on the pituitary may contribute to the differential regulation of FSH and LH secretion in males. In the present study we measured steady state levels of the mRNAs encoding the gonadotropin subunits in pituitary cell cultures treated with 10 nM testosterone (T) as well as in T-treated pituitary cells perifused with pulses of GnRH to explore further the direct actions of T on the pituitary. T treatment of pituitary cells in monolayer culture for 72 h increased FSH beta mRNA 1.5-fold (P less than 0.05), decreased alpha-subunit mRNA to 45% of the control level (P less than 0.05), and decreased LH beta mRNA to 75% of the control level (P less than 0.05). FSH and uncombined alpha-subunit secretion were increased and decreased by T, respectively, whereas basal LH secretion was unchanged. Treatment with 0.1 nM estradiol, a physiological concentration for males, did not change gonadotropin secretion or subunit mRNA concentrations. Between days 2 and 5 in culture in the absence of steroid treatment, steady state levels of LH beta and alpha-subunit mRNA declined (P less than 0.01) 52% and 61%, respectively, but FSH beta mRNA levels were unchanged. Pulsatile stimulation with 2.5 nM GnRH every 1 h for 10 h increased FSH beta mRNA 2.8-fold (P less than 0.05) and increased (P less than 0.05) alpha-subunit mRNA to 117% of the control level. When cell cultures were pretreated with T for 48 h and then perifused with pulses of GnRH, FSH beta, LH beta, and alpha-subunit mRNA levels were 66%, 74%, and 70% of the value during GnRH alone (P less than 0.05). T treatment also reduced (P less than 0.01) the amplitudes of FSH, LH, and alpha-subunit secretory pulses by 18%, 26%, and 41%, respectively. These data indicate that a portion of the negative feedback action of T is at the pituitary to regulate gonadotropin subunit gene expression. Our data reveal two opposing effects of T on FSH beta mRNA: a stimulatory action, which is GnRH independent, and an inhibitory effect, which is related to the actions of GnRH. These divergent actions of T represent one mechanism through which FSH and LH are differentially regulated.

Animals↗
PubMed1992

Effect of gonadotropin-releasing hormone pulse frequency on gonadotropin secretion and subunit messenger ribonucleic acids in perifused pituitary cells.

Slow frequency GnRH pulses have been proposed to preferentially increase circulating FSH levels by increasing FSH synthesis and pulsatile release. Examination of this proposal using various in vivo models, however, has produced conflicting results. To examine directly the effects of GnRH pulse frequency on the pituitary, we compared the effects of 2.5-nM GnRH pulses administered every 1 h or every 4 h vs. no GnRH, using perifused rat pituitary cells. FSH secretion (total area under the response curve) was 2-fold greater (P less than 0.01) with every hour than with every 4 h GnRH pulses. This difference resulted from the increased number of GnRH pulses and increased (P less than 0.05) interpulse FSH secretion, whereas FSH pulse amplitude was unchanged. FSH beta mRNA levels at the completion of the 11-h perifusion were increased 4.5-fold by GnRH every h (P less than 0.01) and 3.3-fold by GnRH every 4 h (P less than 0.05) above levels in untreated cells. FSH beta mRNA levels were greater (P less than 0.05) at the faster GnRH pulse frequency. Because more frequent stimulation delivered more GnRH during the study, cells were next stimulated with 2.5 nM GnRH every 1 h for nine pulses, 7.5 nM GnRH every 4 h for three pulses to equalize the GnRH dose, or 2.5 nM GnRH every 4 h for three pulses. Interpulse FSH secretion and FSH beta mRNA levels were again greater (P less than 0.05) with every hour than every 4 h GnRH pulses. Interpulse LH secretion, FSH and LH pulse amplitude, and LH beta and alpha-subunit mRNA levels were not different between the groups. GnRH doses of 0.1-10 nM every hour increased FSH and LH pulsatile secretion dose-dependently, but FSH beta, LH beta, and alpha-subunit mRNA levels were similar. In conclusion, our data reveal that reducing the frequency of GnRH pulses from every hour to every 4 h reduces both FSH beta mRNA levels and FSH interpulse secretion, but does not change GnRH-stimulated FSH pulsatile release. We suggest that the finding by others that slow frequency GnRH pulses increase circulating FSH levels under certain experimental conditions in vivo may instead be explained by complex hormonal interactions or changes in FSH clearance.

Animals↗
PubMed1992

Changes in the glutathione redox system during ischemia and reperfusion in rat liver.

After 60 min of reperfusion following 60 min of ischemia, the ischemia-induced decrease in liver tissue adenosine triphosphate (ATP) concentration had recovered by 66%, and full recovery of mitochondrial function--that is, the respiratory control index (RCI) and the rate of oxygen consumption in state-III respiration (ST III O2)--was observed. In contrast, liver tissue ATP concentration had recovered by only 13%, and marked low RCI and ST III O2 were observed after 60 min of reperfusion following 180 min of ischemia. Intermediate results were observed in rats after 60 min of reperfusion following 120 min of ischemia. Liver tissue hypoxanthine and xanthine, substrates of xanthine oxidase, increased ischemic time dependently. Liver tissue concentrations of the reduced form of glutathione (GSH) and the oxidized form of glutathione (GSSG) and activities of glutathione peroxidase and glutathione reductase did not change after 60 min of reperfusion following 60 min of ischemia. In contrast, GSH concentration and glutathione peroxidase activity decreased significantly after 60 min of reperfusion following 180 min of ischemia. Since the glutathione redox system is an important contributor to the scavenging of free radicals after reperfusion following a long time of ischemia, the free radical scavenging ability might decrease in spite of enhancement of free radical generation, which might play an important role in the inhibition of the recovery of tissue ATP concentrations and mitochondrial function.

Adenosine Triphosphate↗
PubMed1992

[Inner ear decompression sickness following a scuba dive].

Inner ear decompression sickness (IEDCS) is one form of Type II decompression sickness. Most cases of IEDCS have been associated with saturation dives, so there are very few reports of occurrence following shallow scuba dives. We present here the case of a diver who suffered from IEDCS following a shallow scuba dive (30m), and was successfully treated by the protocol outlined in U.S. Navy treatment table 6. This case suggests that there is the possibility of occurrence of IEDCS, even following a shallow scuba dive, if proper decompression procedures are not adhered to. In addition, detailed analysis of diving profiles should be used to distinguish the inner ear dysfunction seen in some divers from inner ear barotrauma which may be attributable to IEDCS.

Adult↗
PubMed1992

[Asymptomatic multilocular cystic renal cell carcinoma].

From January 1982 to December 1989, we experienced seven multilocular cystic renal cell carcinomas (MLCRCCs) in 36 asymptomatic renal cancers incidentally diagnosed, and none in 23 symptomatic renal cancers (p less than 0.05). No multiocular cystic nephromas (MLCNs) appeared in either group. Though MLCRCCs have been considered to be, in general, extremely rare, they do occur in asymptomatic renal cancers. A multiloculated renal mass with thick septum discovered in an adult by ultrasonography or CT scan should be suspected as being a MLCRCC rather than a MLCN.

Adult↗
PubMed1992

Reduced CD4-CD8 T cell ratios in patients with Wegener's granulomatosis.

All of the patients with Wegener's granulomatosis (WG), whom we studied, exhibited abnormalities in lymphocyte subsets. We used two-color immunofluorescence flow cytometry to examine the lymphocyte subset alterations. WG group showed a decrease in the percentage of CD4+ cells and an increase of CD8+ cells. Within the NK cell family, functionally unidentified CD8+57+ cells were markedly increased in number. The disproportion of these lymphocyte subsets (CD4+ decreases, CD8+57+ increases) was similar to that seen in Acquired Immunodeficiency Syndrome (AIDS) and AIDS related complex (ARC).

Adult↗
PubMed1992

[Laryngeal closure--a simple method and a reversible method for phonation preservation].

Patients with dysphagia due to a disorder in swallowing phase II are candidates for laryngeal closure operation. The operation prevents bolus drainage into the larynx and therefore permits oral feeding. Operative methods in general should be simple and reliable, and furthermore, with regards to this laryngeal closure procedure, they should preferably be reversible to maintain phonatory function, in the event that patients improve swallowing function later on. A laryngeal closure operation which satisfies both conditions has not been previously reported. We present two laryngeal closure operations. One is relatively simple and reliable but irreversible in terms of phonatory function. The other procedure requires more effort but is reversible and therefore allows for preservation of phonatory function. We performed one of these operations on two cases each and obtained good results. 1. Laryngeal closure at the vocal cords. (simple method) The frontal neck skin is incised vertically. The thyroid cartilage perichondrium is incised in the midline and retracted widely on both sides. Then the anterior thyroid lamina is removed at the crico-arytenoid joint. A control hole is opened into the laryngeal lumen by an incision made from the cricoarytenoid membrane to the anterior commissure. The larynx is cut horizontally from the anterior to posterior commissure between the upper and lower lips of the vocal cords. Finally the vocal cords are sutured at the top and bottom of the cut stump. 2. Closure at the false vocal cords. (reversible method for phonation preservation) After the vertical incision has been made, the laryngeal lumen is opened by laryngofissure.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

The primary structure of Aspergillus niger acid proteinase A.

The complete amino acid sequence of the acid proteinase A, a non-pepsin type acid proteinase from the fungus Aspergillus niger var. macrosporus, was determined by protein sequencing. The enzyme was first dissociated at pH 8.5 into a light (L) chain and a heavy (H) chain, and the L chain was sequenced completely. Further sequencing was performed with the reduced and pyridylethylated or aminoethylated derivative of the whole protein, using peptides obtained by digestions with Staphylococcus aureus V8 protease, trypsin, chymotrypsin, and lysylendopeptidase. The location of the two disulfide bonds was determined by analysis of cystine-containing peptides obtained from a chymotryptic digest of the unmodified protein. These results established that the protein consists of a 39-residue L chain and a 173-residue H chain that associate noncovalently to form the native enzyme of 212 residues (Mr 22,265). This is, to our knowledge, the first time that such a protein with a rather short peptide chain associated noncovalently has been found. No sequence homology is found with other acid or aspartic proteinases, except for Scytalidium lignicolum acid proteinase B, an enzyme unrelated to pepsin by sequence, which has about 50% identity with the present enzyme. These two enzymes, however, are remarkably different from each other in some structural features.

Amino Acid Sequence↗