Hongjia L.,Ward of internal medicine |
Hongjia L.,Shandong University |
Qingling G.,Ward of internal medicine |
Meiying L.,Ward of internal medicine |
And 6 more authors.
Cell Biochemistry and Function | Year: 2010
Aberrant innate and adaptive immune responsed to allergens and environmental pollutants lead to respiratory allergic disease such as asthma. In this study, we focused on toll-like receptor-4 (TLR4) expressed on airway epithelium to identify house dust mite (HDM)-regulated allergic inflammation via TLR4 signaling pathway and the triggering to alveolar macrophages (AM)-driven adaptive immune response. The authors found that mouse exposed to HDM showed more eosinophils, neutrophils, monocytes, lymphocytes as well as total cells in bronchoalveolar lavage fluid (BALF) confirmed by flow cytometry. Besides, the expression of TLR4 in airway epithelial cells was significantly increased in both mRNA and protein levels in mice treated with HDM and the expression of CD40 and CD86 in AM was also increased in mice exposed to HDM. Tight correlation between TLR4 protein and CD40, CD86 in AM was identified. This study demonstrates that TLR4 expression on airway epithelium played an essential role in HDM-induced activation of AM in immune responses and allergic inflammation. The airway epithelial TLR4 signaling pathway revealed tight connection between endotoxin exposure and asthma prevalence in the clinic. © 2010 John Wiley & Sons, Ltd. Source
Zheng Y.,Shandong University |
Zheng Y.,Shandong Academy of Sciences |
Wang L.,Shandong Academy of Sciences |
Zhang W.,Secondary Peoples Hospital of Jinan |
And 2 more authors.
BMC Musculoskeletal Disorders | Year: 2012
Background: Studies have demonstrated that carbonic anhydrase I (CA1) stimulates calcium salt precipitation and cell calcification, which is an essential step in new bone formation. Our study had reported that CA1 encoding gene has a strong association with rheumatoid arthritis (RA) and ankylosing spondylitis (AS), two rheumatic diseases with abnormal new bone formation and bone resorption in joints. This study investigated the effect of CA1 on joint inflammation and tissue destruction in transgenic mice that over-express CA1 (CA1-Tg). Methods. CA1-Tg was generated with C57BL/6J mice by conventional methods. CA1-Tg was treated with collagen-II to induce arthritis (CIA). Wild-type mice, CA1-Tg treated with bovine serum albumin (BSA) and transgenic mice over-expressing PADI4 (PADI4-Tg), a gene known to be involved in rheumatoid arthritis, were used as controls. Histochemistry and X-ray radiographic assay were used to examine joint destruction. Western blotting and real time-PCR were used to examine CA1 expression. Results: CIA was observed in 60% of CA1-Tg, 20% of PADI4-Tg and 20% of wild-type mice after collagen injections. No CIA was found in CA1-Tg mice that received injections of BSA. The arthritic score was 5.5 ± 0.84 in the CA1-Tgs but the score was less than 2 in the injected wild-type mice and the PADI4-Tgs. The thickness of the hind paws in the CA1-Tgs was 3.46 ± 0.11 mm, which was thicker than that of PADI4-Tgs (2.23 ± 0.08 mm), wild-type mice (2.08 ± 0.06 mm) and BSA-treated CA1-Tgs (2.04 ± 0.07 mm). Histochemistry showed obvious inflammation, synovial hyperplasia and bone destruction in the joints of CA1-Tg that was not detected in PADI4-Tgs or wild-type mice. X-ray assays showed bone fusion in the paws and spines of CA1-Tg mice. Conclusion: Over-expression of CA1 may aggravate joint inflammation and tissue destruction in the transgenic mice. © 2012 Zheng et al.; licensee BioMed Central Ltd. Source
Hao J.,Shandong Provincial Tumor Hospital |
Dong W.,Shandong Provincial Tumor Hospital |
Xu J.,Shandong Provincial Tumor Hospital |
Yang X.,Shandong Provincial Tumor Hospital |
And 4 more authors.
Chinese Journal of Clinical Oncology | Year: 2011
Objective: To evaluate the clinical effects of the combined late course accelerated hyperfractionation radiotherapy (LCAHR) and chemotherapy on stage III-IVa nasopharyngeal carcinoma (NPC). Methods: A total of 60 NPC patients with stage III-IVa disease were randomly divided into the conventional control group (group A) treated with traditional fractionated radiotherapy, and the study group (group B) treated with LCAHR combined with chemotherapy. A traditional irradiation of 40 Gy at the two opposing facial-cervical anterior-posterior fields (AP-PA) was conducted in both groups, with 20 fractions completed within 4 weeks. After reduction of the irradiated field, LCAHR was performed in group B with a dose of 1.2Gy/f, 2 fractions a day at a 4-6 hour interval, for 14-15 days. The total dose for NPC was 73.6Gy-76Gy in 7 weeks. Chemotherapeutic PF regimen was administered concurrently with radiotherapy. Group A received conventional radiotherapy with a total dose of 70Gy-74Gy for 7-7.5 weeks. Results: The rate of complete regression of NPC was 96.6% (29/30) in group B and 93.3% (28/30) in group A at the end of the course (P>0.05). The 1- and 3-year local control rates in group B and group A were 93.1% and 89.6%, and 82.1% and 67.8%, respectively. The 1- and 3- year survival rates were 96.5% (28/29) and 93.1% (27/29) in group B, and 92.8% (26/28) and 71.4% (20/28) in group A (P< 0.05). The incidence of acute radiation response was obviously higher in group B than in group A. The incidences of long-term adverse reactions, such as dry mouth and fibrosis of the soft tissues of the neck, were lower in group B than in group A. Conclusion: LCAHR can improve the local control rate and the survival rate of NPC patients. Combining LCAHR with chemotherapy can reduce distant metastasis of NPC, with tolerable adverse reactions. Source