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Biomedical subjects

A Saitoh

Publications and source records attributed to A Saitoh.

At least 55 records · Page 3Linked to original sources
PubMed1997

Parameter estimation and dosage adjustment in the treatment with vancomycin of methicillin-resistant Staphylococcus aureus ocular infections.

The susceptibility of methicillin-resistant Staphylococcus aureus (MRSA) to vancomycin (VC) is excellent, but excessive dosing of VC leads to severe side effects. In this study, we present a way of administration planning for each patient based on personal data. To this end, we employed the Sawchuck-Zaske equation to calculate VC clearance (CL) and volume of distribution (Vd) on the basis of three different plasma concentrations of VC, and we used CL and Vd values as prior information before employing the parameter estimation and dosage adjustment program to treat a patient with postsurgical endophthalmitis caused by MRSA and a patient with acute dacryocystitis also caused by MRSA. They had good remissions without any severe side effects.

Acute Disease↗
PubMed1997

Metastasis of breast carcinoma to eyelid and orbit of a postmenopausal woman: good response to tamoxifen therapy.

We report a case of metastatic eyelid and orbital carcinoma in a postmenopausal woman 8 years after mastectomy for cancer. MRI scan T1-weighted images with fat suppression revealed an intraconal lesion surrounding the left optic nerve in addition to the left lid tumor. Excision biopsy demonstrated tumor cells in an Indian file pattern. We diagnosed metastasis of breast carcinoma to the eyelid and orbit. Therapy with tamoxifen reduced eyelid and orbital metastases of carcinoma of the breast. Metastatic breast carcinoma should be listed as one of the causes of lesions of the eyelids.

Adenocarcinoma↗
PubMed1996

Role of spleen or spleen products in the reduced locomotor-enhancing effect of morphine in diabetic mice.

In the present study, we examined the possibility that factor(s) derived from spleen cells are involved in the reduced morphine-induced hyperlocomotion in diabetic mice. The mean total locomotor activity after s.c. administration of morphine (20 mg/kg) in non-diabetic mice was significantly greater than that in diabetic mice. Splenectomized diabetic mice had a significantly higher sensitivity to morphine-induced hyperlocomotion than untreated or sham-operated diabetic mice. However, morphine-induced hyperlocomotion in non-diabetic mice was unaffected by splenectomy or sham-operation. Furthermore, 7 days after adoptive transfer of the supernatant of spleen cell homogenate (SSCH) from diabetic mice (SSCH-D), naive mice that had been injected with SSCH-D showed lower morphine-induced locomotor activity than mice which had been injected with SSCH from non-diabetic mice (SSCH-ND). These results suggest that some factor(s) derived from spleen cells may play an important direct or indirect role in the selective reduction of morphine's locomotor-enhancing effect in diabetic mice.

Animals↗
PubMed1996

Antinociceptive and antitussive effects of morphine in the DA-bg/bg (beige) rat.

Antinociceptive and antitussive effects of morphine were studied in DA-bg/bg (Beige) rats. Intraperitoneal administration of morphine (10 mg/kg) produced a marked antinociceptive effect, in the tail-flick test, in Beige rats and DA rats, a progenitor strain rats. There was no significant difference in the peak antinociceptive effect of morphine between Beige rats and DA rats. The antinociceptive effect of morphine in both Beige rats and DA rats was significantly reduced following pretreatment with a low dose (0.3 mg/kg, i.p.) of naloxone or naltrexonazine (1 mg/kg, s.c.), a selective mu 1-opioid receptor antagonist. Morphine suppressed coughs dose dependently at doses between 0.3-3 mg/kg, i.p., in Beige rats and between 0.1-1.0 mg/kg, i.p., in DA rats. The antitussive potency of morphine in Beige rats was less than that in DA rats. The antitussive effect of morphine was significantly antagonized by pretreatment with naloxone (0.3 mg/kg, i.p.) in both Beige rats and DA rats. However, pretreatment with naltrexonazine (1 mg/kg, s.c.), a selective mu 1-opioid receptor antagonist, had no effect on the antitussive effect of morphine. These results suggest that Beige rats are hyporesponsive to the mu 2-opioid receptor-mediated antitussive effect, but not to the mu 1-opioid receptor-mediated antinociceptive effect.

Analgesics, Opioid↗
PubMed1996

Modification of the effects of 7-OH-DPAT, a dopamine D3-receptor agonist, on morphine-induced hyperlocomotion by diabetes.

We examined the effect of 7-OH-DPAT on spontaneous locomotor activity that is enhanced in diabetic mice. 7-OH-DPAT (0.1-30 mg/kg, s.c.) dose-dependently decreased the enhanced spontaneous locomotor activity in diabetic mice, but not in nondiabetic mice. When mice were pretreated with of 7-OH-DPAT (0.1 mg/kg), morphine-induced enhanced locomotor activity in nondiabetic mice, but not in diabetic mice, was significantly reduced. Furthermore, 7-OH-DPAT (0.1 mg/kg) significantly attenuated the morphine-induced increase in DA turnover in both nondiabetic and diabetic mice. However, DA turnover was significantly greater in diabetic mice than in nondiabetic mice. Thus, it is likely that the enhanced spontaneous locomotor activity in diabetic mice may be partially related to the down-regulation of D3-receptor-mediated modulation of dopamine release in the limbic area.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1996

Involvement of dopamine D2 receptor-mediated functions in the modulation of morphine-induced antinociception in diabetic mouse.

The effects of the dopamine agonists and antagonists on morphine-induced antinociception in diabetic mice were studied. The antinociceptive effect of morphine (5 mg/kg, s.c.) in diabetic mice was significantly less than that in non-diabetic mice. The antinociceptive effect of morphine in diabetic mice, but not that in non-diabetic mice, was significantly enhanced following pretreatment with sulpiride, a selective dopamine D2 antagonist, (30 mg/kg, s.c.). Pretreatment with quinpirole, a selective dopamine D2 agonist, (100 nmol, i.c.v.), markedly increased the antinociceptive effect of morphine in diabetic mice, but not in non-diabetic mice. There was no significant difference in the antinociceptive effect of morphine (5 mg/kg, s.c.) between the quinpirole-treated diabetic mice and saline-treated non-diabetic mice. A higher dose of quinpirole (300 nmol, i.c.v.) had no significant effect on morphine-induced antinociception in diabetic mice. On the other hand, the antinociceptive effect of morphine was significantly reduced by pretreatment with quinpirole (300 nmol, i.c.v.) in non-diabetic mice. Quinpirole (100 and 300 nmol, i.c.v.) dose-dependently increased total locomotor activity in non-diabetic mice. In contrast, a lower dose of quinpirole (100 nmol, i.c.v.) significantly reduced spontaneous locomotor activity in diabetic mice, while a higher dose of quinpirole had no significant effect on the spontaneous locomotor activity. The dopamine turnover ratio in the limbic forebrain and midbrain in diabetic mice were significantly greater than those in non-diabetic mice. When mice were pretreated with quinpirole (100 and 300 nmol, i.c.v), this enhanced dopamine turnover ratio was not observed in either the limbic forebrain or the midbrain of diabetic mice. These findings suggest that the attenuation of morphine-induced antinociception and dopamine D2 receptor-mediated function in diabetic mice may somehow be related.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1996

Sequence variation of the gC gene among pseudorabies virus strains.

We have determined the nucleotide sequences of the major glycoprotein C (gC) gene of 3 pseudorabies virus (PRV) strains isolated in Japan, the USA, and Northern Ireland after gene amplification mediated by a polymerase chain reaction (PCR). The nucleotide and deduced amino acid sequence homologies among the strains were > 98% and > 97%, respectively. The restriction patterns of the amplified DNA fragments generated by restriction endonucleases SalI and SmaI revealed three genomic variations among the 15 PRV strains. The Japanese PRV isolates have identical restriction fragment patterns and differ from those of the non-Japanese isolates examined. Among 3 PRV strains with distinctive genotype each other, there is no significant difference in pathogenicity for the ddY mouse.

Animals↗
PubMed1996

Histologic study of living response to artificially synthesized hydroxyapatite implant: 1-year follow-up.

We implanted artificially synthesized hydroxyapatite spheres into the orbits of 13 rabbits after enucleation. The spheres were removed 1, 2, 3, 6, and 12 months after implantation and examined by light and scanning electron microscopy. Tissue breakdown and exposure of the artificially synthesized hydroxyapatite implants were not observed. Month after month, fibrovascular tissues gradually invaded the pores of the artificially synthesized hydroxyapatite spheres deeper and deeper. Although the hydroxyapatite we used was completely artificially synthesized, we observed a mild foreign-body reaction around the artificially synthesized hydroxyapatite spheres. After 12 months, however, relief of the foreign-body reaction had occurred. Hydroxyapatite spheres for orbital implants after enucleation without scleral enveloping are appropriate.

Animals↗
PubMed1996

Identification and characterization of novel dermal Thy-1 antigen-bearing dendritic cells in murine skin.

Using immunofluorescence on dermal sheets of mouse ear, we identified novel Thy-1+ dermal dendritic cells in murine skin. These cells are resistant to topical corticosteroid treatment. The number of these dermal Thy-1+ dendritic cells is not altered with aging of the mice or with 3 d of culture. Dermal Thy-1+ dendritic cells have melanosomes in their cytoplasm; hence, phagocytic activity is likely to be present. Double immunofluorescence revealed that most of these dermal Thy-1+ dendritic cells express CD45. Furthermore, conventional immunofluorescence and confocal laser scanning microscopic findings showed that most of these Thy-1+ dermal dendritic cells express gamma delta and V gamma 3 T-cell receptors. The relationship between these dermal Thy-1+ dendritic cells and dendritic epidermal T cells is discussed.

Animals↗
PubMed1996

Functional nerve growth factor receptor in von Recklinghausen neurofibromatosis: an immunocytochemical and short-term culture study.

Immunocytochemistry reveals 75 kDa low affinity type nerve growth factor receptor (NGFR) on the cell membrane of human neurofibroma cells of von Recklinghausen disease in vivo and in vitro. NGF-immunoreactivity is detected in the primary and cultured tumor cells. Growth augmentation of cultured neurofibroma cells by exogenous NGF is also confirmed. Phosphotyrosine-immunoreactivity is demonstrated by immunocytochemistry in the in vivo and in vitro neurofibroma cells suggesting possible phosphorylation of tyrosine residue in the NGFR or a cellular protein downstream of signal transduction through the ligand receptor system. These results indicate human neurofibroma cells possess functional NGFR and the growth is potentiated through the NGF-NGFR system in the paracrine and/or autocrine fashion.

Adult↗
PubMed1996

[Two cases of gram-positive sepsis successfully treated with vancomycin in combination with imipenem or cilastatin].

Against gram-positive sepsis, vancomycin (VCM) was administered in combination with imipenem or cilastatin (IPM/CS). Its excellent efficacy was confirmed in 2 cases, one affected with methicillin resistant Staphylococcus aureus and another with Gemella morbillorum. By calculating the FIC index according to a checkerboard technique, the in vitro synergistic effect was also demonstrated. At the present state multi-drug resistant gram-positive infections prevailed, the combination of VCM with IPM/CS can be expected as an effective measure for treating these diseases.

Adolescent↗
PubMed1995

Diagnosis of HIV-1 infection with whole saliva by detection of antibody IgG to HIV-1 with ultrasensitive enzyme immunoassay using recombinant reverse transcriptase as antigen.

Whole-saliva samples were collected from 45 asymptomatic carriers, 18 patients with AIDS-related complex (ARC) or AIDS, and 76 medical students by simple spitting with no stimulation and tested by an ultrasensitive enzyme immunoassay (immune complex transfer enzyme immunoassay) for anti-HIV-1 IgG using recombinant reverse transcriptase as antigen and beta-D-galactosidase as label. With as little as 1 microliter of whole saliva, the lowest signals among the 45 asymptomatic carriers, 8 patients with ARC, and 10 patients with AIDS were 38-, 78-, and 3-fold, respectively, higher than the highest signal among the medical students. When the volume of whole saliva for test was increased up to 100 microliters, no significant effect was observed on signals for seropositive cases and signals for the medical students increased only very slightly. Therefore, whole-saliva samples containing extremely low levels of anti-HIV-1 IgG, even 2,000-fold lower than the lowest level among the 45 asymptomatic carriers tested, were considered to be discriminated from those of seronegative individuals. Thus, the sensitivity and specificity were expected to be both 100% with whole saliva even for a larger number of samples, although the number of samples tested was limited.

Adolescent↗
PubMed1995

Involvement of delta 1-opioid receptors in the antinociceptive effects of mexiletine in mice.

The mechanisms of the antinociceptive effect of mexiletine were assessed by administering selective mu-, delta- and kappa-opioid receptor antagonists in diabetic and non-diabetic mice. Intraperitoneal administration of mexiletine, at doses of 10 and 30 mg/kg, produced dose-dependent antinociception in the tail-pinch test in both non-diabetic and diabetic mice. The antinociceptive effect of mexiletine in diabetic mice was significantly greater than that in non-diabetic mice. The antinociceptive effect of mexiletine did not result from the activation of mu- or kappa-opioid receptors in either non-diabetic or diabetic mice, since treatment with either beta-funaltrexamine, a selective mu- opioid receptor antagonist, or nor-binaltorphimine, a selective kappa-opioid receptor antagonist, was ineffective in blocking mexiletine-induced antinociception. The antinociceptive effect of mexiletine was significantly antagonized by naltrindole, a selective delta-opioid receptor antagonist, in both non-diabetic and diabetic mice. Furthermore, the antinociceptive effect of mexiletine was significantly reduced in both non-diabetic and diabetic mice following pretreatment with 7-benzylidenenaltrexone, a selective delta 1-opioid receptor antagonist, but not with naltriben, a selective delta 2-opioid receptor antagonist. These result suggest that delta 1-opioid receptor-mediated mechanisms may be involved in the antinociceptive effect of mexiletine.

Animals↗
PubMed1995

Stimulation of mouse DNA primase-catalyzed oligoribonucleotide synthesis by mouse DNA helicase B.

Many prokaryotic and viral DNA helicases involved in DNA replication stimulate their cognate DNA primase activity. To assess the stimulation of DNA primase activity by mammalian DNA helicases, we analyzed the synthesis of oligoribonucleotides by mouse DNA polymerase alpha-primase complex on single-stranded circular M13 DNA in the presence of mouse DNA helicase B. DNA helicase B was purified by sequential chromatography through eight columns. When the purified DNA helicase B was applied to a Mono Q column, the stimulatory activity for DNA primase-catalyzed oligoribonucleotide synthesis and DNA helicase and DNA-dependent ATPase activities of DNA helicase B were co-eluted from the column. The synthesis of oligoribonucleotides 5-10 nt in length was markedly stimulated by DNA helicase B. The synthesis of longer species of oligoribonucleotides, which were synthesized at a low level in the absence of DNA helicase B, was inhibited by DNA helicase B. The stimulatory effect of DNA helicase B was marked at low template concentrations and little or no effect was observed at high concentrations. The mouse single-stranded DNA binding protein, replication protein A (RP-A), inhibited the primase activity of the DNA polymerase alpha-primase complex and DNA helicase B partially reversed the inhibition caused by RP-A.

Adenosine Triphosphatases↗
PubMed1995

Antinociceptive effects of the selective non-peptidic delta-opioid receptor agonist TAN-67 in diabetic mice.

The antinociceptive potencies of 2-methyl-4 alpha alpha-(3-hydroxyphenyl)-1,2,3,4,4a,5,12,12 alpha alpha-octahydro-quinolino[2,3,3-g]isoquinoline (TAN-67), a non-peptidic delta-opioid receptor agonist, were examined using the acetic acid abdominal constriction test and the tail-flick test in diabetic mice. TAN-67, at doses of 3-100 mg/kg, s.c. [corrected], produced a marked and dose-dependent inhibition of the number of acetic acid-induced abdominal constrictions in both non-diabetic and diabetic mice. The antinociceptive effect of TAN-67 in the acetic acid abdominal constriction test in diabetic mice was greater than that in non-diabetic mice. Indeed, the ED50 (95% confidence limits) value of TAN-67 for the inhibition of acetic acid-induced abdominal constrictions in diabetic mice (6.0 (3.5-10.5) mg/kg) was significantly lower than that in non-diabetic mice (31.4 (14.2-69.4) mg/kg). The antinociceptive effect of TAN-67 was not antagonized by pretreatment with either beta-funaltrexamine, a selective mu-opioid receptor antagonist, or nor-binaltorphimine, a selective kappa-opioid receptor antagonist. When 7-benzylidenenaltrexone (0.3 mg/kg, s.c.), a selective delta 1-opioid receptor antagonist, was administered 10 min before treatment with TAN-67, the antinociceptive effect of TAN-67 was significantly antagonized. However, naltriben, a selective delta 2-opioid receptor antagonist, had no significant effect on the antinociceptive effect of TAN-67. Furthermore, in the tail-flick test, TAN-67 at doses of 3-30 mg/kg, s.c. [corrected], also produced a marked and dose-dependent antinociceptive effect in diabetic mice, but not in non-diabetic mice. In conclusion, TAN-67 produced an antinociceptive effect through the activation of delta 1-opioid receptors. Furthermore, the results of this study support our hypothesis that mice with diabetes are selectively hyperresponsive to delta 1-opioid receptor-mediated antinociception.

Analgesics↗
PubMed1995

Buprenorphine exerts its antinociceptive activity via mu 1-opioid receptors.

The mechanism of the antinociceptive effect of buprenorphine was assessed by administering selective mu-, mu1--, delta- and kappa-opioid receptor antagonists in mice. Intraperitoneal administration of buprenorphine, at doses of 0.3 to 3 mg/kg, produced dose-dependent antinociception in the tail-flick test. The antinociceptive activity of buprenorphine did not result from the activation of kappa- or delta-opioid receptors, since treatment with either nor-binaltorphimine, a selective kappa-opioid receptor antagonist, or naltrindole, a selective delta-opioid receptor antagonist, was completely ineffective in blocking buprenorphine-induced antinociception. However, the antinociceptive effect of buprenorphine was significantly antagonized by beta-funaltrexamine, a selective mu-opioid receptor antagonist. Moreover, selective mu1-opioid receptor antagonist, naloxonazine and naltrexonazine, also significantly antagonized the antinociceptive effect of buprenorphine. Co-administration of kappa- and delta-opioid receptor antagonist with the mu-opioid receptor antagonists had no significant effect on the antagonistic profiles of the mu-opioid receptor antagonists on the antinociceptive effect of buprenorphine. These results suggest that buprenorphine acts selectively at mu1-opioid receptors to induce antinociceptive effects in mice.

Analgesics, Opioid↗