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1.
Drug Res (Stuttg) ; 66(7): 371-6, 2016 Jul.
Article in English | MEDLINE | ID: mdl-27273710

ABSTRACT

BACKGROUND: Clinical evidences of inhaled salmeterol/fluticasone propionate combination (SFC) therapy are insufficient in early childhood asthma. OBJECTIVES: To examine the effects of SFC50, a combination product of salmeterol xinafoate (50 µg/day) and fluticasone propionate (100 µg/day), in infants and preschool children with asthma. METHODS: The study was conducted at 31 sites in Japan. 35 patients (6 months to 5 years old) with asthma insufficiently controlled by inhaled corticosteroids (100 µg/day) were initiated to treat with SFC50 twice a day for 12 weeks with pressurized metered dose inhalers. The efficacy of SFC50 was assessed using nighttime sleep disorder score as the primary endpoint and the other efficacy measurements. The safety measurement included the incidences of adverse event (AE). RESULTS: Mean patient age was 3.1 years, and 94.2% had mild-to-moderate persistent asthma (atopic type: 65.7%). Nighttime sleep disorder scores, assessed by a nighttime sleep diary, significantly decreased after treatment with SFC50 throughout the study period (p<0.01). SFC50 also significantly improved other efficacy outcomes including asthma symptom score, frequency of short-acting beta-agonist treatment, frequency of unscheduled visits to clinic, frequency of exacerbation due to virus infection, asthma control score and patient QOL score (p<0.01). AEs of cold, upper respiratory inflammation and asthmatic attack occurred in each of the 3 patients (8.6%); however, these were not regarded as treatment-related AEs. CONCLUSIONS: SFC50 improved nighttime sleep disorder score and other efficacy outcome measures with no safety concerns. The results suggest that SFC50 treatment is useful to control the mild-to-moderate asthma in infant and preschool-aged children.


Subject(s)
Adrenal Cortex Hormones/therapeutic use , Asthma/drug therapy , Fluticasone-Salmeterol Drug Combination/therapeutic use , Administration, Inhalation , Adrenal Cortex Hormones/administration & dosage , Anti-Asthmatic Agents/administration & dosage , Anti-Asthmatic Agents/adverse effects , Anti-Asthmatic Agents/therapeutic use , Child, Preschool , Dose-Response Relationship, Drug , Female , Fluticasone-Salmeterol Drug Combination/administration & dosage , Fluticasone-Salmeterol Drug Combination/adverse effects , Humans , Infant , Male , Treatment Outcome
3.
Int J Immunopathol Pharmacol ; 22(3): 707-14, 2009.
Article in English | MEDLINE | ID: mdl-19822087

ABSTRACT

Thalidomide is an effective drug for chronic inflammatory diseases, but the mechanism underlying its immunomodulatory action remains uncertain. Thalidomide has been reported to clinically improve chronic inflammatory granulomatous disorders. In such disorders, the granulomas consist of epithelioid cells, scattered lymphocytes and multinucleated giant cells (MNGC; Langhans-type cells). The present experimental approach permitted the reproduction of MNGC formation from peripheral blood monocytes and examination of thalidomides effect on it. MNGC can be effectively generated from monocytes cultured in the presence of interleukin-4 (IL-4) and macrophage colony-stimulating factor(M-CSF) for 14 days. Thalidomide can inhibit the formation of MNGC in a dose-dependent manner. MNGC formation was partly inhibited by the presence of neutralizing TNF-alpha antibody in the responses induced by IL-4 and M-CSF. Autocrinal TNF-alpha production and modulation of cadhelin expression to regulate cell adhesion might be involved in this inhibitory action of thalidomide. Our results support thalidomides clinical efficacy in the treatment of chronic granulomatous disorders (granulomatosis).


Subject(s)
Anti-Inflammatory Agents/pharmacology , Cell Transdifferentiation/drug effects , Giant Cells, Langhans/drug effects , Granuloma/drug therapy , Monocytes/drug effects , Thalidomide/pharmacology , Antibodies , Autocrine Communication/drug effects , Cells, Cultured , Dose-Response Relationship, Drug , Giant Cells, Langhans/immunology , Giant Cells, Langhans/pathology , Granuloma/immunology , Granuloma/pathology , Humans , Interferon-gamma/metabolism , Interleukin-10/metabolism , Interleukin-1beta/metabolism , Interleukin-4/metabolism , Macrophage Colony-Stimulating Factor/metabolism , Monocytes/immunology , Monocytes/pathology , RNA Interference , Receptors, Tumor Necrosis Factor/genetics , Receptors, Tumor Necrosis Factor/metabolism , Tumor Necrosis Factor-alpha/immunology , Tumor Necrosis Factor-alpha/metabolism
4.
Cancer ; 91(8): 1568-73, 2001 Apr 15.
Article in English | MEDLINE | ID: mdl-11301407

ABSTRACT

BACKGROUND: In the current study, the authors report a 4 year old girl with disseminated retinoblastoma. To find sensitive and specific molecular markers for detection of retinoblastoma cells in blood and marrow, the authors evaluated three photoreceptor-associated gene transcripts by using reverse transcription polymerase chain reaction (RT-PCR). METHOD: Samples of bone marrow and blood were obtained from healthy donors and the patient. RT-PCR was performed to detect the cone alpha'-subunit of cGMP phosphodiesterase (cone alpha'-PDE), the rod beta-subunit of cGMP (rod beta-PDE), and the interphotoreceptor retinoid-binding protein (IRBP) gene transcript in RNA extracted from the samples. RESULTS: While no expression of rod beta-PDE or IRBP was detected in any of the normal samples, expression of cone alpha'-PDE was detected in two out of seven normal marrow samples. Expression of rod beta-PDE was not detected in the patient samples. Expression of IRBP was detected in the patient samples obtained from iliac bone marrow before intensive chemotherapy but not thereafter. CONCLUSION: RT-PCR for IRBP was a useful method for detecting metastatic retinoblastoma cells as well as for evaluating the therapeutic effects of treatment in this particular case.


Subject(s)
Biomarkers, Tumor/analysis , Bone Marrow Neoplasms/secondary , Eye Proteins , Retinoblastoma/pathology , Retinol-Binding Proteins/biosynthesis , Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Bone Marrow Neoplasms/diagnosis , Bone Marrow Neoplasms/genetics , Child, Preschool , DNA Primers , Female , Gene Expression Regulation, Neoplastic , Hematopoietic Stem Cell Transplantation , Humans , Retinoblastoma/drug therapy , Retinoblastoma/genetics , Retinol-Binding Proteins/analysis , Retinol-Binding Proteins/genetics , Reverse Transcriptase Polymerase Chain Reaction
5.
Cancer Res ; 58(9): 1960-4, 1998 May 01.
Article in English | MEDLINE | ID: mdl-9581839

ABSTRACT

pRL1a (IPGLPLSL) is the Ld-binding tumor rejection antigen peptide recognized by CTLs on BALB/c radiation leukemia RL(male)1. We demonstrated that in vivo and in vitro sensitization with pRL1a multiple antigen peptide (MAP), but not with the pRL1a peptide itself, generated pRL1a-specific CTLs in the spleen cells of BALB/c mice. No enhancement of cytotoxicity was observed by emulsifying pRLla MAP in incomplete Freund's adjuvant or in complete Freund's adjuvant for in vivo sensitization. Selective depletion of CD4+ T cells in mice by treatment with anti-L3T4 (CD4) monoclonal antibody and that of macrophages by treatment with carrageenan on in vivo sensitization with pRL1a MAP abrogated CTL generation. The findings suggest that CD4+ T cells and antigen-presenting cells were necessary for the in vivo priming of CD8+ T cells with pRL1a MAP. Furthermore, we demonstrated that in vivo sensitization of BALB/c mice with pRL1a MAP, but not with pRL1a peptide, showed an inhibitory effect on RL(male)1 tumor growth. No growth-inhibitory effect was observed on control RVA, RVD, or Meth A tumors.


Subject(s)
Antigens, Neoplasm/administration & dosage , Leukemia, Experimental/prevention & control , Leukemia, Radiation-Induced/prevention & control , Peptide Fragments/administration & dosage , Vaccination , Animals , Antibodies, Monoclonal/administration & dosage , Antigen-Presenting Cells , Antigens, Neoplasm/immunology , CD4-Positive T-Lymphocytes/immunology , Female , Immunization , Leukemia, Experimental/immunology , Leukemia, Radiation-Induced/immunology , Lymphocyte Activation , Lymphocyte Depletion , Mice , Mice, Inbred BALB C , Peptide Fragments/immunology , Spleen/cytology , Spleen/immunology , T-Lymphocytes, Cytotoxic/immunology , Tumor Cells, Cultured
6.
Nihon Rinsho ; 55(4): 849-54, 1997 Apr.
Article in Japanese | MEDLINE | ID: mdl-9103882

ABSTRACT

Neurologic diseases are common manifestations in enteroviral infections, and most common is aseptic meningitis in children. Only a few percents of poliovirus infected children may result in aseptic meningitis or paralytic poliomyelitis. VAPP (Vaccine Associated Paralytic Poliomyelitis) should be considered among patients with a recent history of receiving OPV (oral polio vaccine). Recently PCR analysis has been used in order to differentiate vaccine-strain from wild-strain poliovirus. There are no specific laboratory findings about enterovirus infections in CNS, however CSF (cerebrospinal fluid) in acute phase may show elevated, predominant polymorphonuclear cells and mean-while shift to mononuclear cell dominance. The G-CSF concentration in CSF with enteroviral meningitis is elevated, which indicates that induced G-CSF is responsible for neutrophil predominance in CSF.


Subject(s)
Enterovirus Infections , Nervous System Diseases , Poliomyelitis , Coxsackievirus Infections , Echovirus Infections , Humans
7.
Rinsho Ketsueki ; 37(2): 95-100, 1996 Feb.
Article in Japanese | MEDLINE | ID: mdl-8852025

ABSTRACT

The function of IgG antibody with regard to L-asparaginase (L-asp) was investigated in vivo. Blood samples were collected before, during and after IV administration of L-asp (6,000 U/sqm for 10 days) in 18 children with acute lymphoblastic leukemia (ALL) previously treated with L-asp. Using enzyme-linked immunosorbent assay (ELISA), serum levels of L-asp and anti-L-asp IgG antibody were measured simultaneously. In 11 cases, the level of anti-L-asp IgG antibody increased prior to, but decreased to within the normal range after drug administration whereas the level of serum L-asp increased after drug administration. In 5 cases, the level of anti-L-asp IgG antibody increased as the level of serum L-asp decreased after drug administration. In contrast, in the 13 cases with no increase in anti-L-asp IgG antibody during L-asp administration, the serum L-asp level was stable. These data indicate that anti-L-asp IgG antibodies play an important role in the immunoclearance of L-asp. We would like to continue to carefully follow patients showing high titers of anti-L-asp IgG antibody during the administration of L-asp.


Subject(s)
Antineoplastic Agents/immunology , Asparaginase/immunology , Immunoglobulin G/physiology , Precursor Cell Lymphoblastic Leukemia-Lymphoma/immunology , Antineoplastic Agents/therapeutic use , Asparaginase/therapeutic use , Child , Child, Preschool , Enzyme-Linked Immunosorbent Assay , Female , Humans , Male , Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy
8.
Miner Electrolyte Metab ; 21(1-3): 171-6, 1995.
Article in English | MEDLINE | ID: mdl-7565443

ABSTRACT

Hypercalcemia accompanied with malignant tumors is generally classified into two categories, namely with or without bone metastasis. As for the latter, bone resorption-stimulating factors produced by tumor cells, such as parathyroid hormone-related protein (PTHrP), show hormone-like effects and promote a bone resorption. Many cases have been reported regarding the production of TPTHrP in adult T cell leukemia (ATL), but few have been reported with acute lymphoblastic leukemia (ALL). We report here a similar case with ALL. A 12-year-old male presented with fever, petechiae and thrombocytopenia, and was diagnosed as ALL. We started the induction therapy and confirmed complete remission. Later, he relapsed 3 times without symptoms apart from hypercalcemia at the beginning. Elevation of the serum calcium level followed by a rise of lymphoblastic cells was recognized. Bone metastasis was excluded since bone mineral density and serum mid region PTH were normal and no abnormal findings were noticed on X rays and 99mTc bone scintigraphy. However, his urinary PTHrP level was high, and his lymphoblastic cells staining immunocytochemically with the monoclonal antibodies against the C-terminal region of PTHrP showed a positively brownish color. Finally, he died of pulmonary aspergillosis. Hypercalcemia was not related to serum PTH or bone metastasis. ATL viral infection reported as a cause of PTHrP production was also excluded from several experimental data. Therefore, we concluded that lymphoblastic cells directly produced PTHrP, and that this PTHrP played an important role in the induction of hypercalcemia.


Subject(s)
Hypercalcemia/metabolism , Neoplasm Proteins/biosynthesis , Precursor Cell Lymphoblastic Leukemia-Lymphoma/metabolism , Protein Biosynthesis , Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Child , Humans , Hypercalcemia/etiology , Male , Parathyroid Hormone-Related Protein , Precursor Cell Lymphoblastic Leukemia-Lymphoma/complications , Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy , Recurrence , Remission Induction
9.
Int J Oncol ; 7(2): 233-8, 1995 Aug.
Article in English | MEDLINE | ID: mdl-21552829

ABSTRACT

The IFN-gamma gene was introduced retrovirally into Meth A cells. IFN-gamma gene infected Meth A (K gamma) cells were highly antigenic and regressed in CB6F(1) mice. Concomitant immunization of CB6F(1), mice with IFN-gamma gene infected Meth A (K gamma) cells after inoculation of parental Meth A protected the mice from parental tumor growth. 1x10(6) infectant Meth A (K gamma) cells protected the mice from growth of 1x10(6) parental Meth A cells, but 2x10(6) infectant cells did not, suggesting that there was an optimal dose of infectant cells for rejection of the parental tumor. Specificity analysis revealed that growth of CMS13 tumor was slightly inhibited by Meth A (K gamma) cells but that of CMS5 was not inhibited. The findings are consistent to those obtained with parental Meth A cells and indicated that the relevant rejection antigen on Meth A (K gamma) cells was identical to the parental Meth A rejection antigen.

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