Biomedical subjects

Hiroaki Takeda

Publications and source records attributed to Hiroaki Takeda.

6 recordsLinked to original sources

PubMed2003

Impaired pulmonary inflammatory responses are a prominent feature of streptococcal pneumonia in mice with experimental emphysema.

Little is known about why patients with chronic obstructive pulmonary disease are susceptible to bacterial infections. Using an animal model of pulmonary emphysema, we investigated the inflammatory responses to bacterial infection. After intratracheal infection with Streptococcus pneumoniae (10(3)-10(7) cfu/mouse), the control mice did not die. However, the mice with emphysema died in a dose-dependent manner. Bronchoalveolar lavage fluid, examined 24 hours after infection showed that the numbers of total cells and neutrophils, in addition to murine tumor necrosis factor-alpha and macrophage inflammatory protein-2 concentrations, were significantly less in the mice with emphysema compared with the control mice. Histopathologic findings revealed that the alveoli were filled with inflammatory cells and exudate in the control mice but not in the mice with emphysema. Seventy-two hours after infection, serum cytokine levels were significantly higher in the mice with emphysema, and significant numbers of S. pneumoniae were detected in both the whole lung tissues and the blood of mice with emphysema. These findings suggest that the inflammatory response in mice with emphysema was impaired at the site of bacterial infection despite the bacteremia, which accelerated severe systemic inflammatory responses. Accordingly, intra-alveolar but not systemic immune responses to bacterial infection were impaired in the presence of experimental emphysema.

Animals↗

PubMed2002

Phosphorylation of Akt/PKB is required for suppression of cancer cell apoptosis and tumor progression in human colorectal carcinoma.

BACKGROUND: Akt/protein kinase B (PKB), which is included in phosphatidyl inositol-3-OH kinase (PI3K) signaling, controls many intracellular processes, such as the suppression of apoptosis and the promotion of the cell cycle. Therefore, the authors investigated phosphorylated Akt (Ser473) in colorectal carcinomas to reveal the role of PI3K signaling during the development of colorectal carcinoma. METHODS: Expression of phosphorylated Akt (Ser473) in two colon carcinoma cell lines (DLD-1 and Colo205) and 65 human colorectal carcinomas was analyzed using western blotting and immunohistochemistry, respectively. Growth inhibition and induction of apoptosis caused by LY294002, a specific inhibitor of PI3K, were also examined in these cell lines. In tumor samples, the level of cell proliferation activity (Ki-67) and number of apoptotic bodies (single stranded DNA) were determined by counting positive cells. RESULTS: LY294002 significantly affected the proliferation and apoptosis of Colo205 cells, suggesting an association with the low phosphorylation level of Akt protein. Immunohistochemic analysis showed that 46% of the tumors had a high level of expression of phosphorylated Akt with a close association with Ki-67 proliferative activity (P < 0.001) and the number of apoptotic bodies (P < 0.001). Akt phosphorylation was also correlated with some clinicopathologic parameters of the malignancies, including depth of invasion, infiltration to venous vessels, lymph node metastasis, and clinicopathologic stage. CONCLUSIONS: The phosphorylated Akt level can monitor cell growth and resistance to apoptosis, indicating that activation of Akt plays an important role during the progression of colorectal carcinomas by helping promote cell growth and rescue cells from apoptosis. These findings also suggest the possibility of using LY294002 for treatment of colorectal carcinoma.

Adult↗

PubMed2002

Expression of the Musashi1 gene encoding the RNA-binding protein in human hepatoma cell lines.

Musashi1, a neural RNA-binding protein, plays an important role in regulating cell differentiation in precursor cells. Recently, expression of Musashi1 has been detected in human tumor tissues such as gliomas and melanomas, suggesting its involvement in oncogenic development. To determine any association between Musashi1 and the development of liver cancer, we investigated its gene expression in seven human hepatoma cell lines: HuH6, HuH7, Hep3B, SK-Hep1, HepG2, HLE, and HLF. Musashi1 mRNA expression was analyzed using the reverse-transcription polymerase chain reaction (PCR), and the PCR products were sequenced using a subcloning procedure. Musashi1 protein expression was analyzed in HuH7 and HepG2 cells by Western blot and immunofluorescence staining. Musashi1 mRNA was detected in the HuH6, HuH7, and Hep3B hepatoma cell lines, but not in the others. Sequencing of the PCR-amplified Musashi1 cDNA in these three cell lines showed the expected sequence of the human Musashi1 gene. Musashi1 protein expression was confirmed in HuH7 cells, which were positive for Musashi1 mRNA expression, but not in HepG2 cells. These results suggest that Musashi1 expression may be an important factor in the development of several types of carcinoma such as human hepatoma, and may be a useful molecular marker for tumor detection.

Animals↗

PubMed2002

A patient with adult Still's disease with an increased Chlamydia pneumoniae antibody titer.

Adult Still's disease is an important differential diagnosis of pyretic disease and it does not necessarily appear to be a distinct disease entity. The etiology of adult Still's disease is not yet known. However, it has been considered that adult Still's disease may be triggered by certain infections, such as the Coxsackie, parvo B19, rubella, mumps, Epstein-Barr, and cytomegalo virus, as well as mycoplasma, toxoplasma, and so on. Recently, we experienced a patient with adult Still's disease with an increased Chlamydia pneumoniae antibody titer. The titer decreased slowly after the beginning of steroid therapy, associated with improvement of clinical symptoms. In this report we mention the relationship between the pathogenesis of adult Still's disease and a high titer of Chlamydia pneumoniae antibody.

Adult↗

PubMed2002

Effect of lipopolysaccharide on peptide transporter 1 expression in rat small intestine and its attenuation by dexamethasone.

BACKGROUND/AIM: The peptide transporter (PepT1) activity is upregulated or preserved under certain pathological conditions. The aim of this study was to investigate the PepT1 expression during lipopolysaccharide (LPS) treatment and the effect of dexamethasone on PepT1 expression. METHODS: Rats were injected daily for 3 days with (1) LPS; (2) LPS plus dexamethasone; (3) dexamethasone, and (4) saline only. Mucosal specimens were used for Northern blot and Western blot analyses. Tissues of small intestine were taken for histological studies. In addition, tumor necrosis factor alpha and interleukin 1 beta levels were determined 3 h after single injections of the above mediators. RESULTS: Northern blot analysis revealed that LPS treatment significantly decreased the expression of mRNA for PepT1 (32-62% of controls) at different time points. In the LPS + dexamethasone group, it was 66-95% of controls. The protein level of PepT1 in the jejunum was consistent with the mRNA expression level. Immunohistochemistry also showed a reduction of PepT1 immunoreactivity in the LPS group. LPS treatment resulted in increased tumor necrosis factor alpha and interleukin 1 beta levels, but dexamethasone treatment profoundly counteracted the cytokine production. CONCLUSIONS: This is the first report that LPS treatment reduces PepT1 expression in the rat small intestine. Short-term treatment with dexamethasone attenuated the effects of LPS by decreasing the cytokine levels.

Animals↗

PubMed2002

[Malabsorption].

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