Feng Hua

Fudan University, Shanghai, Shanghai Shi, China

Are you Feng Hua?

Claim your profile

Publications (4)8.51 Total impact

  • Feng Hua, Xiang Wang, Lei Zhu
    [Show abstract] [Hide abstract]
    ABSTRACT: BACKGROUND: Recent clinical data suggest that treatment with terlipressin (TP) may be more advantageous for septic shock than catecholamines. However, it is unknown whether TP would be effective for acute respiratory distress syndrome (ARDS) patients with shock. OBJECTIVES: The aim of this study was to compare the impact of TP vs. dopamine on hemodynamic variables and vascular endothelial growth factor (VEGF) in ARDS patients with shock. METHODS: We studied 32 ARDS patients with shock despite fluid loading, who were randomized to receive TP (16 patients) or dopamine (16 patients). TP was administered as a continuous intravenous dose of 1.3 μg/kg/h and dopamine was administered in doses up to 20 μg/kg/min to maintain a mean arterial pressure of 70 ± 5 mm Hg for 48 h. Hemodynamic changes, ratio of partial pressure of arterial oxygen to fraction of inspired oxygen (PaO(2)/FiO(2)), and VEGF were recorded prospectively. RESULTS: There was a significant correlation between the plasma VEGF level and the lung injury score at baseline (r = 0.387, p < 0.01). VEGF concentrations significantly decreased from baseline levels in the TP group (p < 0.05) at 48 h; there was no difference in the dopamine group (p > 0.05) at 48 h vs. baseline. There was no significant difference in the tumor necrosis factor-α concentration between the groups. Conclusions: TP treatment has the potential to inhibit VEGF and improve oxygenation in patients with shock in the early stage of ARDS.
    Journal of Emergency Medicine 08/2012; · 1.33 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Lipopolysaccharides (LPSs) activate the innate immune response during Gram-negative bacterial infections through the Toll-like receptor 4 (TLR4)/myeloid differentiation protein 2 (MD-2) complex. MD-2 binds LPS with high affinity and is critical for TLR4-dependent signal transduction. However, the exact role of MD-2 on LPS signal transduction and cytokine production in alveolar macrophages (AMs) remains unclear. This study showed that the transcription levels of MD-2, TLR4 and MyD88 in the NR8383 cell line were up-regulated after LPS stimulation and that the increased transcript levels were attenuated after RNA interference of MD-2. Similarly, LPS induced increases in TNF-α, IL-1β and IL-6 protein levels in NR8383 cell supernatants was significantly inhibited by MD-2 silencing. These results suggest that in association with the TLR4/MyD88 signaling pathway LPS-induced cytokine production can be partially reduced by MD-2 silencing in the rat pulmonary alveolar macrophage cell line NR8383. MD-2 silencing was proved to be a useful tool for testing the role of MD-2 in the LPS signaling pathway and may be a potential therapeutic tool against LPS-induced lung inflammation.
    Immunology letters 08/2011; 141(1):94-101. · 2.91 Impact Factor
  • Feng Hua, Weiying Ren, Lei Zhu
    [Show abstract] [Hide abstract]
    ABSTRACT: Mice lacking plasminogen activator inhibitor-1 (PAI-1) did not affect lung injury induced by gram-positive bacteria pneumococcal pneumonia but worsened lung injury induced by gram-negative bacteria Klebsiella. The exact mechanisms have not been completely elucidated. In this study, we examined the signaling pathway of Toll-like receptor 4 (TLR4) with/without PAI-1 in acute lung injury (ALI) induced by lipopolysaccharides (LPS) in mice. PAI-1 knockout mice (n=60) and wild-type mice (n=60) were exposed to LPS intratracheal instillation. Different groups of mice were then sacrificed at 0 and 8 h after LPS instillation. PAI-1-/- mice showed increased excess lung water and elevated cytokines production and release. In addition, expression of TLR4 was up-regulated and the phosphorylation activation of extracellular regulating kinase (ERK) and c-Jun N-terminal kinase (JNK) were also increased in PAI-1 knockout mice compared to wild-type mice. Inversely, interleukin (IL)-1 receptor-associated kinase-M (IRAK-M) and suppressor of cytokine signaling 1 (SOCS1) were both significantly reduced in PAI-1-/-mice after LPS challenge. PAI-1 deletion increased lung injury induced by LPS through up-regulation of TLR4, ERK and C-JNK and down-regulation of TLR4 negative regulators.
    Blood coagulation & fibrinolysis: an international journal in haemostasis and thrombosis 05/2011; 22(6):480-6. · 1.25 Impact Factor
  • Source
    Feng Hua, Lei Zhu
    [Show abstract] [Hide abstract]
    ABSTRACT: The association of Kikuchi Fujimoto disease (KFD) with cryptogenic organizing pneumonia (COP) is extremely rare. We report a case of simultaneous diagnosis of KFD and COP. A 33-year-old male presented with a 1-month cough illness and fever lasting for 5 days. The chest radiograph revealed double lower lobe infiltrate, which was unresponsive to antibiotics. A cervical lymph node was first found in the development of this disease. Bronchoscopy, bronchoalveolar lavage and lung biopsy established the diagnosis of COP, while a lymph node biopsy was consistent with KFD. The patient improved on steroids. KFD and COP are possible part of a disease continuum, rather than separate entities.
    BMC Infectious Diseases 03/2010; 10:64. · 3.03 Impact Factor