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Biomedical subjects

S Harada

Publications and source records attributed to S Harada.

At least 577 records · Page 32Linked to original sources
PubMed1985

Cephabacin M1-6, new 7-methoxycephem antibiotics of bacterial origin. II. Isolation, characterization and structural determination.

Six components of new cephem antibiotics, cephabacin M1-6, were isolated from the culture filtrate of Xanthomonas lactamgena YK-431 by various types of column chromatographies and preparative reverse-phase HPLC. Their structures were determined by spectroscopic analyses and degradation studies. They consist of 7-methoxydeacetylcephalosporin C as a nucleus and a tri- to heptapeptide including a new amino acid, which is bound at the 3-position with an ester bond.

Anti-Bacterial Agents↗
PubMed1985

Interactions of formylamino- and methoxy-substituted beta-lactam antibiotics with beta-lactamases.

Cephem and nocardicin-type monocyclic beta-lactam antibiotics with a formylamino substituent were highly resistant to hydrolysis by both penicillinases and cephalosporinases. Among antibiotics with a methoxy substituent, an N-sulfonated monocyclic beta-lactam antibiotic, sulfazecin was resistant to beta-lactamases, but cephem antibiotics were sensitive to the cephalosporinase of Enterobacter cloacae. The resistance of the antibiotics to the beta-lactamases depended primarily on the presence of the substituent, but affinity for the beta-lactamases was affected not only by the substituent but also by the presence of other side chains. Formylamino compounds and sulfazecin were as good inducers of beta-lactamases as semisynthetic 7-methoxycephalosporins, but naturally occurring 7-methoxycephalosporins were poor inducers. The inducer activities of the antibiotics were not necessarily related to their beta-lactamase stabilities. The stabilities of the compounds to the beta-lactamases were well reflected in their antibacterial activities against beta-lactamase producing bacteria.

Anti-Bacterial Agents↗
PubMed1985

Inclusion compounds of lankacidin-group antibiotics with cyclodextrins.

Lankacidin-group antibiotics formed inclusion compounds with beta-cyclodextrin in molar ratios of about 1:1. These compounds showed remarkably improved water-solubility and stability in aqueous solutions. The structure of the inclusion compounds of lankacidin A is proposed based on the facility of their inclusion with beta-cyclodextrin and the results of 1H NMR spectral studies.

Anti-Bacterial Agents↗
PubMed1985

Necrotizing lymphoid vasculitis in X-linked lymphoproliferative syndrome.

An 8-year-old maternally related relative of three boys who had developed agammaglobulinemia associated with Epstein-Barr virus (EBV)-induced infectious mononucleosis was studied for X-linked lymphoproliferative syndrome (XLP) in 1979. At that time, he demonstrated no striking immunologic aberrations and was seronegative for EBV. Subsequently, immunologic abnormalities including failure to switch from IgM to IgG antibody synthesis after secondary immunization with bacteriophage phi X174 were detected. In 1983, he experienced episodic intracerebral hemorrhages, with the second being fatal. At autopsy, necrotizing vasculitis and aneurysms involving arteries of the central nervous system were observed. Studies of blood obtained immediately before and after death failed to show antibodies to EBV. However, EBV genome was demonstrated in tissues obtained at autopsy by DNA hybridization studies. Fatal lymphoid vasculitis in this patient is unique among boys with XLP in the registry. These findings probably extend the phenotypic expressions of XLP.

Antibodies, Viral↗
PubMed1985

Quantitative analysis of AIDS-related virus-carrying cells by plaque-forming assay using an HTLV-I-positive MT-4 cell line.

Quantitation of acquired immune deficiency syndrome (AIDS)-related virus-bearing cells was analyzed by a newly developed plaque-forming assay. A chemically adherent HTLV-I-positive MT-4 cell monolayer was used as the cytolytic responder cells to the AIDS-virus infection. When AIDS-virus-infected cells (Molt-4/HTLV-III, H9/HTLV-III, and CEM/LAV) were seeded with MT-4 cells, plaques were observed corresponding to the number of HTLV-III-positive cells plated. Plaque formation was inhibited by the addition of anti-HTLV-III-positive serum (neutralizing antibody) to the agarose medium. These data suggest that this plaque-forming assay technique should be useful for the quantitative analysis of AIDS-virus-bearing cells.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Correlation between high susceptibility to AIDS virus and surface expression of OKT-4 antigen in HTLV-I-positive cell lines.

Most human T-cell lymphotropic virus type I (HTLV-I)-carrying cell lines possess high susceptibility to AIDS retrovirus. This high permissiveness was clearly correlated with the amount of OKT-4 molecules, the possible receptor for AIDS retrovirus, expressed on the cell surface of HTLV-I-bearing cell lines. However, no correlation was noted in HTLV-I-negative cell lines.

Antigens, Surface↗
PubMed1985

Role of Epstein-Barr virus in the etiology of Burkitt's lymphoma.

Although Epstein-Barr virus (EBV) was discovered in cultured Burkitt's lymphoma (BL) cells, its exact role remains unclear. Viral genome is found in 95-98% of endemic BL and 15-20% of non-endemic BL. Children destined to develop BL in Africa show elevated titres of viral capsid antibodies one to two years preceding emergence of BL. A multistep process follows early EBV infection during early childhood. Immune deficiency probably permits continuation of the infections, with smouldering polyclonal B-cell proliferation proceeding. Final steps in the pathogenesis consist of cytogenetic and molecular conversion to monoclonal BL. Reciprocal chromosomal translocations involve breakpoints containing c-myc, heavy- and light-chain Ig loci. Activation of oncogenes, c-myc and B-lym, may be essential in the molecular pathogenesis of BL. A spectrum of EBV-induced pathological entities is found in individuals with X-linked lymphoproliferative and acquired immune deficiency syndromes. Lymphoma identical to endemic BL occurs in these immune-deficient patients. Non-endemic BL is possibly due to immune defects, initiators and promoters of B-cell proliferation, which may not be identical to factors in endemic BL; however, cytogenetic events and activation of oncogenes may be pathways of both endemic and non-endemic BL.

Acquired Immunodeficiency Syndrome↗
PubMed1985

[Evaluation of ototoxic effect of micronomicin by intravenous drip infusion].

Ototoxic effect of micronomicin (MCR) in intravenous drip administration was investigated in guinea pigs (300--400 g) receiving MCR for 30 days at dose of 50 and 100 mg/kg, respectively. MCR was dissolved in physiologic saline and 1.5 ml of the solution was infused through polyethylene tube into the left external jugular vein with Perista mini-pump for 60 minutes every day after measurement of body weight. Auditory impairment was monitored by pinna reflex audiometry. Pinna reflex loss was not detected in any animal in frequency range (0.5 to 20 kHz). Cochlear hair cell damage generally was of mild degree. Two out of 6 animals treated with MCR 50 mg/kg (Table 1) showed outer hair cell loss confined to unilateral basal end and posterior 3/4 of the first turn, respectively. Outer hair cell loss was noticed in 4 of 9 animals receiving MCR 100 mg/kg (Table 2); much less extensive in 3 animals, unsymmetrical slightly extensive in remaining 1. Unilateral circumscribed loss of inner hair cells was noticed at lower part of the hook in the latter one. Vestibular hair cell loss was scattered and less extensive and occurred in 4 of the 6 50 mg/kg given animals and in 7 of the 9 100 mg/kg ones. Comparison in incidence and extension of the outer hair cell loss of the cochlea (Tables 3, 4) in the present study and previous ones on the ototoxic effect of MCR in intramuscular and intravenous administration suggests that there was no distinct difference in enhancement of the ototoxic effect in the intravenous drip administration.

Aminoglycosides↗
PubMed1985

[Clinical evaluation of lenampicillin in the treatment of superficial suppurative skin and soft tissue infection. A double-blind study comparing amoxicillin].

A double-blind controlled clinical study between lenampicillin (LAPC), a newly developed oral ampicillin (ABPC) prodrug, and amoxicillin (AMPC) was conducted for the treatment of suppurative skin and soft tissue infection as grouped in 6 disease types. LAPC or AMPC were orally administered at a daily dose of 1,000 mg, in 4 equally divided doses. Each group was treated for 14 days. The results indicated that LAPC was equal to AMPC in evaluations of effectiveness and usefulness, although incidence of severe side effects was slightly lower in LAPC. The number of cases studied was 235 (115 in the LAPC group, 120 in the AMPC group). Among these, 10 patients (4 in LAPC, 6 in AMPC) were excluded and 12 patients (5 in LAPC, 7 in AMPC) dropped out. Final global improvement rating was evaluated in 213 patients (106 in LAPC, 107 in AMPC). General usefulness rating was evaluated in 215 patients (106 in LAPC, 109 in AMPC), and overall safety rating was evaluated in 231 patients (115 in LAPC, 116 in AMPC). Final global improvement rating of LAPC was, "cured", 55.7% and "cured" and "remarkably improved", 79.2%. The rate increased to 88.7% when "improved" was included. On the other hand, in the AMPC group, "cured" was 50.5%, and "cured" and "remarkably improved" was 76.6%. The rate increased to 91.6% when "improved" was included. No significant difference was found between the 2 drug groups. In overall safety rating of LAPC, "safe" was 93.9%, while in the AMPC group, "safe" was 94.0%. No significant difference was found between the 2 drug groups. Side effects were noted in 2 of 115 patients (1.7%) among the LAPC group and in 5 of 116 patients (4.3%) among the AMPC group. Incidence of severe side effects was slightly lower in LAPC (P less than 0.1). General usefulness rating of LAPC was, "remarkably useful", 56.6% and the rate increased to 86.8% when "useful" was included. In the AMPC group, "remarkably useful" was 51.4%, and increased to 84.4% when "useful" was included. No significant difference was found between the 2 drug groups.

Adult↗
PubMed1985

Inflammatory mediators and modulators released in organ culture from rabbit skin lesions produced in vivo by sulfur mustard. I. Quantitative histopathology; PMN, basophil, and mononuclear cell survival; and unbound (serum) protein content.

When applied topically to the skin of rabbits in vivo, sulfur mustard (SM), the vesicant used in World War I, produced a slowly developing inflammatory response, which peaked in size at 1 and 2 days, ulcerated within 3 days, and reepithelialized by 10 days. Histologically, basophils and polymorphonuclear leukocytes (PMNs) were common in both early and late lesions, and the crust over the ulcers was composed of dead epidermal cells, fibrin, and large numbers of PMNs. Healing occurred under the crust by migration of epidermal cells from the margins of the lesions and from the hair follicles. In organ culture, the lesion explants survived well, and reepithelialization even took place. Their excellent survival enabled us to compare the life spans of the infiltrating leukocytes within an inflammatory site. PMNs within the explants began disappearing during the first day of culture, and almost all had disappeared by 3 days. In contrast, over half of the basophils and the mononuclear cells within the explants were still present after 3 days of culture. The 1-, 2-, 3-, 6-, and 10-day (1.0-sq cm) SM lesion biopsies showed a 30-45% increase in weight (when compared with normal skin), presumably due to the extravasation of serum proteins and the fluids retained by them. When the biopsies were organ-cultured for 3 days, the 1-, 2-, and 3-day lesions lost weight, and the 6- and 10-day lesions (and normal skin) gained weight. These weight differences were not due to the amount of unbound protein extractable into the culture fluids, because both the early lesions and the late lesions contained about the same amount of unbound protein. The most likely explanation for these weight differences is that the newly formed ground substances of late lesions absorbed culture fluid, because the ground substance had changed from the sol state of acute inflammation (in which it was extractable) back to its normal gel state (in which it was not extractable). The unbound protein extractable into the culture fluids was mostly of serum origin. This protein averaged 1.9 mg for 1.0 sq cm normal skin explants (with a mean weight of 215 mg), and 6.4 mg for 1-day SM lesions (with a mean weight of 313 mg). Because rabbit serum contains about 60 mg protein/ml, these figures indicate that normal skin contained about 15% (unbound) serum by weight.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

Inflammatory mediators and modulators release in organ culture from rabbit skin lesions produced in vivo by sulfur mustard. II. Evans blue dye experiments that determined the rates of entry and turnover of serum protein in developing and healing lesions.

Extravasated serum seems to be the major modulator of the local inflammatory response, because it provides both proinflammatory and antiinflammatory components. This report describes the rates of entry and turnover of extravasated serum protein in dermal inflammatory lesions produced by the military vesicant sulfur mustard (SM). Rabbits, bearing SM skin lesions, were given an intravenous injection of Evans blue dye, so that at the time of sacrifice, 2 hours later, their skin lesions were 2 hours and 1,2,3,6, and 10 days of age. Evans blue labels serum albumin, a representative serum protein. By multiplying the amount of Evans blue contained in the lesions by a factor that converted micrograms of Evans blue into milligrams of serum protein, the authors could estimate the 2-hour rate of entry of serum protein into these lesions. Serum protein in the lesions was both bound and unbound. The unbound protein was extractable from the lesions into the culture fluids, and, electrophoretically, was similar in composition to serum protein. Grossly edematous peak lesions (1 day of age) contained 7.8 mg of unbound serum protein per square centimeter of skin. Healing lesions (6 and 10 days of age) contained about 4.5 mg/sq cm, and normal skin about 1.7 mg/sq cm. Lesions 1 day of age had the highest rate of serum albumin entry, and about 36% of this Evans-blue-labeled protein was unbound, ie, extractable into the culture fluids. Lesions 3 and 6 days of age had a rate of serum albumin entry that was roughly half that of 1-day lesions, and only about 13% of this entering protein was unbound. Normal skin had a very low rate of serum albumin entry, and only 8% of this entering protein was unbound. The turnover rate of the unbound (extractable) serum protein could be estimated from the 2-hour entry rate of the Evans-blue-labeled albumin and the total protein in the culture fluids. In 1-day lesions, about 25% of the serum protein in the culture fluids was protein which had entered during the last 2 hours, so that 100% of this unbound protein should have been replaced once in 8 hours. In contrast, in 3- and 6-day lesions, this unbound serum protein should have been replaced once in about 35 hours, and in normal skin once in 80 hours. Evans-blue-labeled serum albumin continuously entered both the bound and unbound compartments of the SM lesions, even during the healing stages.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

Dissociation of creatine kinase activity from hydrolytic enzyme activities in muscle of dystrophic mice.

Time course studies were done to reexamine the age-dependency of intramuscular enzymatic changes in dystrophic mice. Most of the activities of hydrolytic enzymes in dystrophic mice were elevated in comparison to the controls throughout the span of 8 weeks which was examined. In contrast, the activity of creatine kinase remained depressed throughout the same period. This tendency was similarly seen in the muscles of forelimb and hindlimb but not in heart muscle. The observations are compatible with the notion that the increased activities of hydrolytic enzymes are causally related to the destruction of muscular tissue, leading to the malfunction of contractile machinery in the dystrophic muscles.

Animals↗