Low frequency spin dynamics in undoped and Sr-doped La2CuO4.
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Journal Article↗
Biomedical subjects
K Yoshimura
Publications and source records attributed to K Yoshimura.
Adenovirus-mediated augmentation of cell transfection with unmodified plasmid vectors.
The present study demonstrates that the human adenovirus (Ad) can augment transfer and expression of a gene within plasmid DNA unmodified by nonspecific linkers or by linker-ligand complexes. Following the transfection of COS-7 cells with pRSVL, a luciferase expression plasmid vector directed by the Rous sarcoma virus-long terminal repeat promoter, luciferase activity in the target cells was 10(3)- to 10(4)-fold higher when the cells were also infected with Ad-CFTR, a replication-deficient recombinant Ad containing human cystic fibrosis transmembrane conductance regulator (CFTR) cDNA. The enhancement of luciferase gene expression in COS-7 cells was also observed with Ad-dl312 (a replication-deficient E1a deletion mutant Ad with no exogenous gene) and wild type Ad5. The efficiency of cell transfection with pRSVL in the presence of an Ad was achieved in a dose-dependent fashion with progressively higher luciferase activity in cells infected by increasing amounts of Ad-CFTR, Ad-dl312, or Ad5. The augmentation by Ad-CFTR of the transfer and expression of the luciferase gene in cells was similar to that of another transfection reagent, cationic liposomes. Further, when Ad-CFTR and liposomes were used in combination, 4- to 100-fold more efficient expression of the luciferase gene was achieved than with Ad-CFTR or liposomes alone. When COS-7, HeLa, and CV-1 cells were evaluated in parallel in the presence or absence of liposomes, Ad-mediated enhancement of luciferase activity was observed in all cell lines. Thus, exposure of target cells to replication-deficient or competent human Ad will markedly augment transfer and expression of the genes within plasmid DNA in mammalian cells in vitro without modifying the plasmid with linkers or linker-ligand complexes, a strategy that should be useful for in vitro and in vivo gene transfer applications.
Adenoviridae↗
Alternative splicing of intron 23 of the human cystic fibrosis transmembrane conductance regulator gene resulting in a novel exon and transcript coding for a shortened intracytoplasmic C terminus.
The cystic fibrosis transmembrane conductance regulator (CFTR) gene, the gene responsible for the lethal hereditary disorder cystic fibrosis, codes for a membrane protein functioning as a cAMP-regulated Cl- channel. Evaluation of human CFTR mRNA transcripts from epithelial and nonepithelial cells demonstrated a CFTR cDNA containing a 260-base pair (bp) insertion between the known CFTR exons 23 and 24, introducing a premature stop codon that would result in a CFTR protein shortened by 61 amino acids at the carboxyl terminus compared to that expected from the normal reported human CFTR coding sequences. Sequence analysis of intron 23 of the CFTR gene demonstrated that the 260-bp insertion (named exon 24a), a part of the reported intron 23 and located consecutive to exon 24, is likely generated by an alternative splice acceptor site. The exon 24a+ CFTR mRNA transcripts represented 3-16% of the total CFTR transcripts in epithelial and nonepithelial cells. These observations suggest an unexpected plasticity of expression of the CFTR gene, where alternative splicing of precursor CFTR mRNA transcripts permits the use of an alternative exon derived from a genomic segment previously believed to function as an intron.
Alternative Splicing↗
Sequential bypass for multisegmental occlusive disease.
We evaluated the effectiveness of a sequential bypass for multisegmental occlusive disease. Forty-seven multiple bypass grafts were performed on 43 patients ranging in age from 55 to 83 years (mean: 70 years). The indications for operation included incapacitating claudication in 20 limbs, resting pain in 15, and nonhealing ulcers in 12. An anatomical arterial bypass was performed on 36 limbs, consisting of an aorto-femoro-popliteal bypass in 21 limbs, a femoro-popliteal-posterior tibial bypass in 8, an ilio-femoro-popliteal bypass in 4, an ilio-femoro-posterior tibial bypass in 2, and a femoro-popliteal-plantar bypass in 1. Similarly, an extra-anatomical arterial bypass was performed on 11 limbs, consisting of an axillo-femoro-popliteal bypass in 6, a crossover femoro-femoro-popliteal bypass in 3, an axillo-femoro-posterior tibial bypass in 1, and a crossover femoro-femoro-anterior tibial bypass in 1. The follow-up period ranged from 3 to 77 months (mean: 23 months). Twelve graft failures occurred, and 2 of them required major amputations. The cumulative graft patency rate was 85% at one year and 65% at 3 years. Arterial Doppler examination revealed a mean preoperative ankle-brachial index of 0.29 +/- 0.25. The early and late mean postoperative ankle-brachial indices, however, increased to 0.97 +/- 0.19 and 0.84 +/- 0.25, respectively. Midterm results have indicated that such multiple sequential bypass grafts are effective.
Aged↗
Antigen dependent release of interleukin 5 in vitro from spleen cells of mice infected with Angiostrongylus cantonensis.
The kinetics of eosinophil growth and/or survival stimulating factors (Eo-stimulating factors) released by spleen cells from A. cantonensis-infected mice were assessed by in vitro marrow cultures. When spleen cells from C57BL/6 mice 8 to 20 days p.i. were cultured with young adult A. cantonensis worm antigen or Con A, almost equal amounts of Eo-stimulating factors were detected in the conditioned media obtained from both stimulations. No Eo-stimulating factor activity was detected in cultures from spleen cells without stimulation or from normal spleen cells with stimulation. Production of Eo-stimulating factors was inhibited by the pretreatment of the spleen cells with anti-Thy1.2 or anti-L3T4 antibodies plus complement but not with anti-Lyt2.2 antibody. In the presence of anti-mouse IL-5 monoclonal antibody, the activity of Eo-stimulating factors was inhibited by up to 99%. IL-5, therefore, appears to play a principal role in induction of eosinophilia in mice infected with A. cantonensis.
Angiostrongylus cantonensis↗
The effect of cyclosporin A on Angiostrongylus cantonensis infection and eosinophilia in mice.
Male BALB/c mice were infected with Angiostrongylus cantonensis and at various times p.i. treated with cyclosporin A (CsA) either for 5 days continuously or intermittently, or for 12-16 days on alternate days. They were monitored for peripheral blood eosinophilia and at necropsy examined for CSF and bone marrow eosinophilia, and worm recovery. CsA treatment provoked a transient inhibition of peripheral blood eosinophilia in all groups examined, followed by rebounding eosinophilia. There was no significant difference in bone marrow and CSF eosinophilia between CsA- and vehicle-treated groups. Mice treated with CsA on alternate days yielded lower intracranial worm recovery with small-sized worms at days 7, 21 and 30 p.i. than vehicle-treated groups did. No significant reduction in worm recovery was noted in mice treated for 5 days either continuously or intermittently, although worms, especially female ones, harvested from groups treated with CsA from days--1 to 3 or from days 13 to 17 were significantly smaller than those from vehicle-treated groups. CsA-treatment suppressed blastogenic responses of spleen cells against Con A or worm antigen at days 7 and 21 p.i. In vitro treatment of the 3rd stage larvae with CsA did not adversely influence survival of A. cantonensis in mice. These data indicate that CsA exerts anti-parasitic effects against A. cantonensis in mice.
Angiostrongylus cantonensis↗
Physical dependence on morphine induced in dogs via the use of miniosmotic pumps.
The difference between the development of physical dependence on morphine administered via Alzet miniosmotic pumps as well as syringe injection (twice a day) at fixed times was examined in conscious dogs. Physical dependence was quantified by polygraphically measuring naloxone-precipitated withdrawal signs on the day 8 after the subcutaneous implantation of miniosmotic pumps which supplied morphine at 1-5 mg/kg/day. Morphine plasma levels were maintained at 19-25 and 41-47 ng/mL during infusions of morphine at doses of 2.5 and 5 mg/kg/day, respectively. Morphine withdrawal was characterized by hyperactivity, biting, digging, tremors, nausea, hyperthermia, and increased wakefulness, and by electroencephalographic (EEG) activation in the amygdala and hippocampus, followed by dissociation of the EEG in the cortex (fast wave) from that in the limbic (slow wave) system, increased heart rates, and raised blood pressure. These morphine withdrawal signs seemed to be more severe than those exhibited in animals that had received syringe injections of morphine at the same doses. These results suggest that the use of miniosmotic pumps in dogs may be a very convenient and useful method for both evaluating drug dependence and studying its mechanisms.
Animals↗
Strongyloides ratti: dissociation of immunological memory of the protection against tissue migrating larvae and intestinal adult worms in mice.
Immunological memory generated by infection with S. ratti was studied separately in the migratory and intestinal phases in mice. Protection against reinfection in the migratory phase was 96-98% at 2 weeks but significantly decreased to 60% at 12 weeks after the primary infection. However, protection in the intestinal phase was 96% even 12 weeks after the primary infection. Recall of immunity against the intestinal phase persists for longer than that against the migratory phase in mice.
Animals↗
Transient retention of Strongyloides ratti in the caecal mucosa during infection in mice.
Adult worms of Strongyloides ratti, after elimination from the small intestine, were retained in the caecum for at least three days during the infection in mice. This retention was a biological event but not due to a simple mechanical trapping in faeces. In addition to the local mucosal mastocytosis, eosinophil infiltration was remarkable in the caecum around day 10 when adult worms were expelled from there.
Animals↗
Structural and functional characterization of Sec66p, a new subunit of the polypeptide translocation apparatus in the yeast endoplasmic reticulum.
SEC66 encodes the 31.5-kDa glycoprotein of the Sec63p complex, an integral endoplasmic reticulum membrane protein complex required for translocation of presecretory proteins in Saccharomyces cerevisiae. DNA sequence analysis of SEC66 predicts a 23-kDa protein with no obvious NH2-terminal signal sequence but with one domain of sufficient length and hydrophobicity to span a lipid bilayer. Antibodies directed against a recombinant form of Sec66p were used to confirm the membrane location of Sec66p and that Sec66p is a glycoprotein of 31.5 kDa. A null mutation in SEC66 renders yeast cells temperature sensitive for growth. sec66 cells accumulate some secretory precursors at a permissive temperature and a variety of precursors at the restrictive temperature. sec66 cells show defects in Sec63p complex formation. Because sec66 cells affect the translocation of some, but not all secretory precursor polypeptides, the role of Sec66p may be to interact with the signal peptide of presecretory proteins.
Amino Acid Sequence↗
Demonstration of human papillomavirus type 1 DNA in a wart with bowenoid histologic changes.
A verrucous lesion on the forearm of a 6-year-old boy was found to be a human papillomavirus type 1 (HPV-1)-induced wart. In addition to typical intracytoplasmic inclusion bodies, the specific cytopathogenic effect of HPV-1 infection, bowenoid changes, were noted on histopathological examination.
Bowen's Disease↗
Varied clinical morphology of HPV-1-induced warts, depending on anatomical factors.
The clinical and histological features of 49 lesions induced by human papillomavirus type 1 (HPV-1) were studied. The majority of cases showed the typical clinical features and location of such lesions. They were usually located on the ventral or lateral surfaces of the hands or feet, and were dome-shaped lesions with a central depression. However, HPV-1-induced lesions located on other body areas displayed different clinical features, such as those of common warts, a digitate wart, and a cutaneous horn. One lesion on a healing burn scar had a herpes-like appearance. As these 49 lesions were induced by the same type of HPV (HPV-1), differences in their clinical features are likely to have been due to host-related factors.
Adolescent↗
Different susceptibility to the IL-3 induced-protective effects between Strongyloides ratti and Nippostrongylus brasiliensis in C57BL/6 mice.
Repetitive administration of recombinant IL-3 induced protection against Strongyloides ratti but not against Nippostrongylus brasiliensis in C57BL/6 mice. Numbers of S. ratti were negligible from day 4 to day 6 post-infection in mice injected with IL-3, whereas N. brasiliensis burdens were almost equal from day 4 to day 6 between mice injected with IL-3 or with medium. Mice treated with IL-3 and then concurrently infected with S. ratti and N. brasiliensis were protected from intestinal S. ratti but not from N. brasiliensis. The numbers of intestinal mucosal mast cells were increased by the repetitive IL-3 treatment on one day after the final injection and was augmented by subsequent infection with both nematodes.
Animals↗
Ablation of eosinophils with anti-IL-5 antibody enhances the survival of intracranial worms of Angiostrongylus cantonensis in the mouse.
Effects of depressed eosinophilia on the development of Angiostrongylus cantonensis in the mouse were studied using monoclonal rat anti-mouse-interleukin-5 antibody (anti-IL-5). The administration of anti-IL-5 strongly depressed peripheral, cerebrospinal fluid (CSF) and medullary eosinophilic responses in mice infected with A. cantonensis, when compared with groups treated with phosphate-buffered saline solution (PBS) alone or isotype-matched rat IgG. There was no significant difference in A. cantonensis antigen specific IgG and IgE antibody responses between rat IgG treated and anti-IL-5 treated mice. Intracranial worm recovery in anti-IL-5 treated mice was consistently high throughout the course of the study and some worms migrated from the brain to the lungs. By contrast, almost all the intracranial worms in the mouse groups treated with PBS alone or rat IgG died before day 32. These data clearly indicate that IL-5 is essential for eosinophil responses in A. cantonensis infected mice and also that eosinophils serve as a potential effector cell in the killing of the intracranial worms in mice.
Angiostrongylus cantonensis↗
Familial clustering of human T lymphotropic virus type 1 uveitis.
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Adult↗
Leukotriene B4 induces lung injury in the rabbit: role of neutrophils and effect of indomethacin.
The effects of exogenous leukotriene B4 (LTB4) on the pulmonary microvascular permeability and the roles of polymorphonuclear (PMN) leukocytes and the cyclooxygenase products of arachidonic acid in the microvascular response to LTB4 in the isolated non-blood-perfused rabbit lungs were studied. Microvascular permeability and lung edema were evaluated by use of the fluid filtration coefficient (Kf) and the wet-to-dry lung weight ratio (W/D ratio), respectively. Pulmonary capillary pressure was estimated by the double occlusion technique. We studied five groups of lungs: lungs were given 1) both PMN leukocytes and a bolus injection of LTB4 (5 micrograms, n = 6), 2) LTB4 alone (n = 5), 3) PMN leukocytes alone (n = 5), 4) control vehicles (n = 5), or 5) indomethacin (40 micrograms/ml) before PMN leukocytes and LTB4 (n = 6). We observed that LTB4 increased Kf and W/D ratio in the presence of PMN leukocytes in the perfusate without affecting the pulmonary arterial and capillary pressures. Neither LTB4 alone nor PMN leukocytes alone produced changes in Kf and W/D ratio. Indomethacin failed to inhibit the LTB4-induced increases in Kf and W/D ratio. These results suggest that LTB4 produces lung injury that is dependent on PMN leukocytes but not on the cyclooxygenase pathway of arachidonic acid metabolism.
Animals↗
Father-son testicular cancer.
Testicular tumors in closely related family members are rare. We report a case of familial testicular cancer occurring in father-son pairs. The father had teratocarcinoma and his son developed pure seminoma. The association of a genetic factor in the etiology of testicular malignancy is discussed.
Adult↗
[Pathogenesis of idiopathic interstitial pneumonia/idiopathic pulmonary fibrosis: cellular and molecular biology of the disease].
Idiopathic interstitial pneumonia (IIP), which is referred to as "idiopathic pulmonary fibrosis (IPF)" in US and European countries or "cryptogenic fibrosing alveolitis (CFA)" in UK, is considered to result from an uncontrolled, chronic inflammatory process in the lower respiratory tract and alveoli of the lung. It is conceivable that some hereditary background may contribute to the disease in susceptible individuals. In IPF, alveolitis involving activation of alveolar macrophages (AM), neutrophils, T- and B-lymphocytes and/or other inflammatory cell types precedes the injury to the lung parenchyma and interstitial fibrosis. Activation and accumulation of cellular components in the disease seem to be modulated by a variety of biological substances such as cytokines, chemotactic factors and adhesion molecules. Exposure to inorganic dusts or viral infection also may trigger activation of AM. The injury to the alveolar epithelium, capillary endothelial cells and extracellular matrix mediated by oxidants and/or proteases produced by AM and neutrophils results in the derangement of the lung parenchyma. Subsequent fibrotic change of the lung interstitium is characterized by the accumulation of mesenchymal cells such as fibroblasts and deposition of their connective tissue produces within the alveolar walls. In this process, AM is considered to play a major role by secreting growth factors for mesenchymal cells, although alveolar epithelial and endothelial cells also seem to participate in activating mesenchymal cell proliferation in IPF. Possibly, connective tissue synthesis and/or degradation may be altered in the process of IPF, although there is no direct evidence for this so far. Thus, IPF is a chronic inflammatory disease in which inflammatory processes of the alveoli injure the lung parenchyma and modulate the proliferation of mesenchymal cells which result in the fibrotic change. The pathogenesis of the disease involves multiple cellular components of the lower respiratory tract through modulation of gene expression and protein synthesis of a variety of biological factors.
Gene Expression Regulation↗