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Lawrence G. Morawa - One of the best experts on this subject based on the ideXlab platform.

  • The roles of monocytic heat shock protein 60 and Toll-like receptors in the regional Inflammation Response to wear debris particles.
    Journal of biomedical materials research. Part A, 2010
    Co-Authors: Hsiao-nan Hao, Bingrong Zheng, Sam Nasser, Weiping Ren, Michael Latteier, Paul H. Wooley, Lawrence G. Morawa
    Abstract:

    The biological Response to orthopaedic wear debris is central to peri-prosthetic tissue Inflammation and osteolysis, through mechanisms that include local inflammatory cytokine production. In particular, interleukin-1 beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha|) are generated in high quantities following monocyte accumulation in periprosthetic inflammatory tissue, and these cytokine combine with other inflammatory mediators to trigger osteolysis. Since the precise mechanisms involved in debris-associated Inflammation remain unclear, it is important to understand how wear debris particles initially interact with inflammatory cells. We have previously demonstrated that the severity of the Inflammation Response is influenced by the size, shape, and quantity of particles accumulated in tissues. The current in vitro and in vivo results indicate that heat-shock protein (Hsp) expression is elevated when monocytes are exposed to wear debris particles. We have also addressed the mechanisms by which heat-shock protein 60 (Hsp60) positively modulates inflammatory cytokines via Toll-like receptor-4 (TLR4) signal transduction pathway on mononuclear cells. Furthermore, down-regulation of TLR4 expression using antisense oligonucleotides targeted to TLR4 mRNA suppressed cytokine production in both exogenous Hsp60 and particles stimulated cultures. Collectively, these data indicate that monocytic Hsp60 is an additional inducible immunoregulatory mediator in Response to particle-induced cell stress.

  • The roles of monocytic heat shock protein 60 and Toll-like receptors in the regional Inflammation Response to wear debris particles.
    Journal of biomedical materials research. Part A, 2010
    Co-Authors: Hsiao-nan Hao, Bingrong Zheng, Sam Nasser, Weiping Ren, Michael Latteier, Paul H. Wooley, Lawrence G. Morawa
    Abstract:

    The biological Response to orthopaedic wear debris is central to peri-prosthetic tissue Inflammation and osteolysis, through mechanisms that include local inflammatory cytokine production. In particular, interleukin-1 β (IL-1β) and tumor necrosis factor-α (TNF-α|) are generated in high quantities following monocyte accumulation in periprosthetic inflammatory tissue, and these cytokine combine with other inflammatory mediators to trigger osteolysis. Since the precise mechanisms involved in debris-associated Inflammation remain unclear, it is important to understand how wear debris particles initially interact with inflammatory cells. We have previously demonstrated that the severity of the Inflammation Response is influenced by the size, shape, and quantity of particles accumulated in tissues. The current in vitro and in vivo results indicate that heat-shock protein (Hsp) expression is elevated when monocytes are exposed to wear debris particles. We have also addressed the mechanisms by which heat-shock protein 60 (Hsp60) positively modulates inflammatory cytokines via Toll-like receptor-4 (TLR4) signal transduction pathway on mononuclear cells. Furthermore, down-regulation of TLR4 expression using antisense oligonucleotides targeted to TLR4 mRNA suppressed cytokine production in both exogenous Hsp60 and particles stimulated cultures. Collectively, these data indicate that monocytic Hsp60 is an additional inducible immunoregulatory mediator in Response to particle-induced cell stress. © 2009 Wiley Periodicals, Inc. J Biomed Mater Res, 2010

Hsiao-nan Hao - One of the best experts on this subject based on the ideXlab platform.

  • The roles of monocytic heat shock protein 60 and Toll-like receptors in the regional Inflammation Response to wear debris particles.
    Journal of biomedical materials research. Part A, 2010
    Co-Authors: Hsiao-nan Hao, Bingrong Zheng, Sam Nasser, Weiping Ren, Michael Latteier, Paul H. Wooley, Lawrence G. Morawa
    Abstract:

    The biological Response to orthopaedic wear debris is central to peri-prosthetic tissue Inflammation and osteolysis, through mechanisms that include local inflammatory cytokine production. In particular, interleukin-1 beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha|) are generated in high quantities following monocyte accumulation in periprosthetic inflammatory tissue, and these cytokine combine with other inflammatory mediators to trigger osteolysis. Since the precise mechanisms involved in debris-associated Inflammation remain unclear, it is important to understand how wear debris particles initially interact with inflammatory cells. We have previously demonstrated that the severity of the Inflammation Response is influenced by the size, shape, and quantity of particles accumulated in tissues. The current in vitro and in vivo results indicate that heat-shock protein (Hsp) expression is elevated when monocytes are exposed to wear debris particles. We have also addressed the mechanisms by which heat-shock protein 60 (Hsp60) positively modulates inflammatory cytokines via Toll-like receptor-4 (TLR4) signal transduction pathway on mononuclear cells. Furthermore, down-regulation of TLR4 expression using antisense oligonucleotides targeted to TLR4 mRNA suppressed cytokine production in both exogenous Hsp60 and particles stimulated cultures. Collectively, these data indicate that monocytic Hsp60 is an additional inducible immunoregulatory mediator in Response to particle-induced cell stress.

  • The roles of monocytic heat shock protein 60 and Toll-like receptors in the regional Inflammation Response to wear debris particles.
    Journal of biomedical materials research. Part A, 2010
    Co-Authors: Hsiao-nan Hao, Bingrong Zheng, Sam Nasser, Weiping Ren, Michael Latteier, Paul H. Wooley, Lawrence G. Morawa
    Abstract:

    The biological Response to orthopaedic wear debris is central to peri-prosthetic tissue Inflammation and osteolysis, through mechanisms that include local inflammatory cytokine production. In particular, interleukin-1 β (IL-1β) and tumor necrosis factor-α (TNF-α|) are generated in high quantities following monocyte accumulation in periprosthetic inflammatory tissue, and these cytokine combine with other inflammatory mediators to trigger osteolysis. Since the precise mechanisms involved in debris-associated Inflammation remain unclear, it is important to understand how wear debris particles initially interact with inflammatory cells. We have previously demonstrated that the severity of the Inflammation Response is influenced by the size, shape, and quantity of particles accumulated in tissues. The current in vitro and in vivo results indicate that heat-shock protein (Hsp) expression is elevated when monocytes are exposed to wear debris particles. We have also addressed the mechanisms by which heat-shock protein 60 (Hsp60) positively modulates inflammatory cytokines via Toll-like receptor-4 (TLR4) signal transduction pathway on mononuclear cells. Furthermore, down-regulation of TLR4 expression using antisense oligonucleotides targeted to TLR4 mRNA suppressed cytokine production in both exogenous Hsp60 and particles stimulated cultures. Collectively, these data indicate that monocytic Hsp60 is an additional inducible immunoregulatory mediator in Response to particle-induced cell stress. © 2009 Wiley Periodicals, Inc. J Biomed Mater Res, 2010

Tao Hou - One of the best experts on this subject based on the ideXlab platform.

  • Systemic Inflammation Response Index (SIRI) Independently Predicts Survival in Advanced Lung Adenocarcinoma Patients Treated with First-Generation EGFR-TKIs.
    Cancer management and research, 2021
    Co-Authors: Shun Jiang, Yuhua Feng, Sisi Wang, Xianling Liu, Qianqian Wang, Chao Deng, Tao Hou
    Abstract:

    Background Systemic Inflammation Response index (SIRI) has been reported to be an effective blood-based biomarker for predicting prognosis in various kinds of cancer patients. However, the prognostic role of SIRI in advanced lung adenocarcinoma patient remains unclear. Methods The aim of the present study is to evaluate the prognostic role of SIRI in EGFR-mutant advanced lung adenocarcinoma patients treated with first-generation EGFR-TKIs. A total of 245 patients who received gefitinib, erlotinib, or icotinib at the Second Xiangya Hospital were retrospectively evaluated. SIRI was defined as neutrophil count×monocyte/lymphocyte count. The optimal cut-off value was determined according to receiver operation characteristic curve analysis. Characteristics of patients were compared via chi-square test or Fisher's exact test. Survivals were estimated by the Kaplan-Meier method and compared by the Log rank test. Multivariate analysis was estimated using the Cox proportional hazards model. Results It is showed that high SIRI was associated with male patient, smoker, worse ECOG PS, 19-DEL mutation. Kaplan-Meier survival analysis showed that ECOG PS, brain metastasis, SIRI were significantly correlated with progression-free survival (PFS), and gender, ECOG PS, brain metastasis, NLR and SIRI were significantly correlated with overall survival (OS). Multivariate analysis showed that SIRI and ECOG PS independently predict PFS and OS. Conclusion Our findings indicate that SIRI is an effective and convenient marker for predicting prognosis in advanced EGFR-mutant lung adenocarcinoma patients treated with first-generation TKI.

  • Systemic Inflammation Response Index Is a Predictor of Poor Survival in Locally Advanced Nasopharyngeal Carcinoma: A Propensity Score Matching Study.
    Frontiers in oncology, 2020
    Co-Authors: Yuhua Feng, Na Zhang, Sisi Wang, Wen Zou, Ping Liu, Xianling Liu, Tao Hou
    Abstract:

    Introduction Nasopharyngeal carcinoma (NPC) is a common malignancy in China and known prognostic factors are limited. In this study, neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), systemic immune Inflammation index (SII), and systemic Inflammation Response index (SIRI) were evaluated as prognostic factors in locally advanced NPC patients. Materials and Methods NPC patients who received curative radiation or chemoradiation between January 2012 and December 2015 at the Second Xiangya Hospital were retrospectively reviewed, and a total of 516 patients were shortlisted. After propensity score matching (PSM), 417 patients were eventually enrolled. Laboratory and clinical data were collected from the patients' records. Receiver operating characteristic curve analysis was used to determine the optimal cut-off value. Survival curves were analyzed using the Kaplan-Meier method. The Cox proportional hazard model was used to identify prognostic variables. Results After PSM, all basic characteristics between patients in the high SIRI group and low SIRI group were balanced except for sex (p=0.001) and clinical stage (p=0.036). Univariate analysis showed that NLR (p=0.001), PLR (p=0.008), SII (p=0.001), and SIRI (p

Bingrong Zheng - One of the best experts on this subject based on the ideXlab platform.

  • The roles of monocytic heat shock protein 60 and Toll-like receptors in the regional Inflammation Response to wear debris particles.
    Journal of biomedical materials research. Part A, 2010
    Co-Authors: Hsiao-nan Hao, Bingrong Zheng, Sam Nasser, Weiping Ren, Michael Latteier, Paul H. Wooley, Lawrence G. Morawa
    Abstract:

    The biological Response to orthopaedic wear debris is central to peri-prosthetic tissue Inflammation and osteolysis, through mechanisms that include local inflammatory cytokine production. In particular, interleukin-1 beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha|) are generated in high quantities following monocyte accumulation in periprosthetic inflammatory tissue, and these cytokine combine with other inflammatory mediators to trigger osteolysis. Since the precise mechanisms involved in debris-associated Inflammation remain unclear, it is important to understand how wear debris particles initially interact with inflammatory cells. We have previously demonstrated that the severity of the Inflammation Response is influenced by the size, shape, and quantity of particles accumulated in tissues. The current in vitro and in vivo results indicate that heat-shock protein (Hsp) expression is elevated when monocytes are exposed to wear debris particles. We have also addressed the mechanisms by which heat-shock protein 60 (Hsp60) positively modulates inflammatory cytokines via Toll-like receptor-4 (TLR4) signal transduction pathway on mononuclear cells. Furthermore, down-regulation of TLR4 expression using antisense oligonucleotides targeted to TLR4 mRNA suppressed cytokine production in both exogenous Hsp60 and particles stimulated cultures. Collectively, these data indicate that monocytic Hsp60 is an additional inducible immunoregulatory mediator in Response to particle-induced cell stress.

  • The roles of monocytic heat shock protein 60 and Toll-like receptors in the regional Inflammation Response to wear debris particles.
    Journal of biomedical materials research. Part A, 2010
    Co-Authors: Hsiao-nan Hao, Bingrong Zheng, Sam Nasser, Weiping Ren, Michael Latteier, Paul H. Wooley, Lawrence G. Morawa
    Abstract:

    The biological Response to orthopaedic wear debris is central to peri-prosthetic tissue Inflammation and osteolysis, through mechanisms that include local inflammatory cytokine production. In particular, interleukin-1 β (IL-1β) and tumor necrosis factor-α (TNF-α|) are generated in high quantities following monocyte accumulation in periprosthetic inflammatory tissue, and these cytokine combine with other inflammatory mediators to trigger osteolysis. Since the precise mechanisms involved in debris-associated Inflammation remain unclear, it is important to understand how wear debris particles initially interact with inflammatory cells. We have previously demonstrated that the severity of the Inflammation Response is influenced by the size, shape, and quantity of particles accumulated in tissues. The current in vitro and in vivo results indicate that heat-shock protein (Hsp) expression is elevated when monocytes are exposed to wear debris particles. We have also addressed the mechanisms by which heat-shock protein 60 (Hsp60) positively modulates inflammatory cytokines via Toll-like receptor-4 (TLR4) signal transduction pathway on mononuclear cells. Furthermore, down-regulation of TLR4 expression using antisense oligonucleotides targeted to TLR4 mRNA suppressed cytokine production in both exogenous Hsp60 and particles stimulated cultures. Collectively, these data indicate that monocytic Hsp60 is an additional inducible immunoregulatory mediator in Response to particle-induced cell stress. © 2009 Wiley Periodicals, Inc. J Biomed Mater Res, 2010

Sam Nasser - One of the best experts on this subject based on the ideXlab platform.

  • The roles of monocytic heat shock protein 60 and Toll-like receptors in the regional Inflammation Response to wear debris particles.
    Journal of biomedical materials research. Part A, 2010
    Co-Authors: Hsiao-nan Hao, Bingrong Zheng, Sam Nasser, Weiping Ren, Michael Latteier, Paul H. Wooley, Lawrence G. Morawa
    Abstract:

    The biological Response to orthopaedic wear debris is central to peri-prosthetic tissue Inflammation and osteolysis, through mechanisms that include local inflammatory cytokine production. In particular, interleukin-1 beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha|) are generated in high quantities following monocyte accumulation in periprosthetic inflammatory tissue, and these cytokine combine with other inflammatory mediators to trigger osteolysis. Since the precise mechanisms involved in debris-associated Inflammation remain unclear, it is important to understand how wear debris particles initially interact with inflammatory cells. We have previously demonstrated that the severity of the Inflammation Response is influenced by the size, shape, and quantity of particles accumulated in tissues. The current in vitro and in vivo results indicate that heat-shock protein (Hsp) expression is elevated when monocytes are exposed to wear debris particles. We have also addressed the mechanisms by which heat-shock protein 60 (Hsp60) positively modulates inflammatory cytokines via Toll-like receptor-4 (TLR4) signal transduction pathway on mononuclear cells. Furthermore, down-regulation of TLR4 expression using antisense oligonucleotides targeted to TLR4 mRNA suppressed cytokine production in both exogenous Hsp60 and particles stimulated cultures. Collectively, these data indicate that monocytic Hsp60 is an additional inducible immunoregulatory mediator in Response to particle-induced cell stress.

  • The roles of monocytic heat shock protein 60 and Toll-like receptors in the regional Inflammation Response to wear debris particles.
    Journal of biomedical materials research. Part A, 2010
    Co-Authors: Hsiao-nan Hao, Bingrong Zheng, Sam Nasser, Weiping Ren, Michael Latteier, Paul H. Wooley, Lawrence G. Morawa
    Abstract:

    The biological Response to orthopaedic wear debris is central to peri-prosthetic tissue Inflammation and osteolysis, through mechanisms that include local inflammatory cytokine production. In particular, interleukin-1 β (IL-1β) and tumor necrosis factor-α (TNF-α|) are generated in high quantities following monocyte accumulation in periprosthetic inflammatory tissue, and these cytokine combine with other inflammatory mediators to trigger osteolysis. Since the precise mechanisms involved in debris-associated Inflammation remain unclear, it is important to understand how wear debris particles initially interact with inflammatory cells. We have previously demonstrated that the severity of the Inflammation Response is influenced by the size, shape, and quantity of particles accumulated in tissues. The current in vitro and in vivo results indicate that heat-shock protein (Hsp) expression is elevated when monocytes are exposed to wear debris particles. We have also addressed the mechanisms by which heat-shock protein 60 (Hsp60) positively modulates inflammatory cytokines via Toll-like receptor-4 (TLR4) signal transduction pathway on mononuclear cells. Furthermore, down-regulation of TLR4 expression using antisense oligonucleotides targeted to TLR4 mRNA suppressed cytokine production in both exogenous Hsp60 and particles stimulated cultures. Collectively, these data indicate that monocytic Hsp60 is an additional inducible immunoregulatory mediator in Response to particle-induced cell stress. © 2009 Wiley Periodicals, Inc. J Biomed Mater Res, 2010