OBJECTIVE: Keloids are exuberant cutaneous scars that form due to abnormal growth of fibrous tissue following an injury. The primary aim of this study was to assess the efficacy and mechanism of hyperbaric oxygen therapy (HBOT) to reduce the keloid recurrence rate after surgical excision and radiotherapy. METHODS: (1) A total of 240 patients were randomly divided into two groups. Patients in the HBOT group (O group) received HBOT after surgical excision and radiotherapy. Patients in the other group were treated with only surgical excision and radiotherapy (K group). (2) Scar tissue from recurrent patients was collected after a second operation. Hematoxylin and eosin (H&E) staining was used to observe keloid morphology. Certain inflammatory factors (interleukin-6 (IL-6), hypoxia-inducible factor-1α (HIF-1α), tumor necrosis factor-α (TNF-α), nuclear factor κB (NF-κB), and vascular endothelial growth factor (VEGF)) were measured using immunohistochemical staining. RESULTS: (1) The recurrence rate of the O group (5.97%) was significantly lower than that of the K group (14.15%), P<0.05. Moreover, patients in the O group reported greater satisfaction than those in the K group (P<0.05). (2) Compared with the recurrent scar tissue of the K group, the expression levels of the inflammatory factors were lower in the recurrent scar tissue of the O group. CONCLUSIONS Adjunctive HBOT effectively reduces the keloid recurrence rate after surgical excision and radiotherapy by improving the oxygen level of the tissue and alleviating the inflammatory process.
Adolescent ; Adult ; Female ; Humans ; Hyperbaric Oxygenation ; Hypoxia-Inducible Factor 1, alpha Subunit/blood* ; Inflammation ; Interleukin-6/blood* ; Keloid/surgery* ; Male ; Middle Aged ; NF-kappa B p50 Subunit/blood* ; Perfusion ; Recurrence ; Surveys and Questionnaires ; Tumor Necrosis Factor-alpha/blood* ; Vascular Endothelial Growth Factor A/blood* ; Young Adult

<b>OBJECTIVEb>To pinpoint angiogenesis- and lymphangiogenesis-related genes in nasopharyngeal carcinoma (NPC).

<b>METHODSb>Based on the reported microarray data which identified 831 differentially expressed genes in NPC tissues and the latest genomic information, we selected 246 genes for analysis with the smallest differential expression threshold of 260. Gene function analysis and network construction was carried out based on literature mining for analysis of the signaling pathways related with angiogenesis and lymphangiogenesis of NPC.

<b>RESULTSb>The 246 genes were related with such keywords as nasopharyngeal carcinoma, EB virus, metastasis, angiogenesis, lymphangiogenesis, and invasion. Particularly, we found that up to 52 genes were associated with angiogenesis (P=0.00001), and 19 genes form 12 related gene pairs (P=0.0042). Twenty-one lymphangiogenesis-related genes were identified (P=0.00001), and 6 of these genes formed a gene network (P=0.0226). Eight genes, including PTGS2, participated in the nuclear factor-&kappa;B (NF-&kappa;B) pathway, which was closely related to angiogenesis in small cell lung cancer (P=7.87E-07). Five genes, including STAT1 and CXCL10, participated in toll-like receptor signaling pathway (P=0.00176).

<b>CONCLUSIONb>PTGS2 and NF-&kappa;B promote angiogenesis of NPC, and the role of toll-like receptor signaling pathway in lymphangiogenesis warrants further investigation.

Carcinoma ; Carcinoma, Squamous Cell ; blood supply ; genetics ; pathology ; Cyclooxygenase 2 ; metabolism ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Humans ; Lymphangiogenesis ; NF-kappa B p50 Subunit ; metabolism ; Nasopharyngeal Neoplasms ; blood supply ; genetics ; pathology ; Neovascularization, Pathologic ; Oligonucleotide Array Sequence Analysis ; Signal Transduction ; Toll-Like Receptors ; metabolism

<b>OBJECTIVEb>To explore the impact of inflammation, water metabolism and immune function on the establishment of a mouse model of damp-heat syndrome with MHV-A59 infection.

<b>METHODSb>Twenty-four mice were randomly divided into control group, virus group, damp-heat group and model group. The peripheral blood CD4(+) and CD8(+) lymphocytes were detected by flow cytometry, and the serum levels of IFN-γ and IL-4 were assayed by ELISA. The expressions of NF-&kappa;B and AQP4 in the liver and stomach were determined using immunohistochemistry.

<b>RESULTSb>The expression of NF-&kappa;B and CD4(+)/CD8(+) ratio in the virus and model groups were significantly higher than those in the damp-heat and control groups, while the expression of AQP4 was significantly higher in the model and damp-heat groups than in the other groups. Compared with the control group, the model group showed a significantly higher ratio of IFN-γ/IL-4.

<b>CONCLUSIONSb>MHV-A59 virus is the main cause of elevated NF-&kappa;B expression and CD4(+)/CD8(+)/ ratio, while damp-heat syndrome is responsible for increased AQP4 expression, and their synergistic effect results in increased IFN-γ/IL-4 ratio. The mouse model established using MHV-A59 virus and the damp-heat factors can mimic damp-heat syndrome described in traditional Chinese medicine theory.

Animals ; Aquaporin 4 ; metabolism ; CD4-CD8 Ratio ; Disease Models, Animal ; Hepatitis, Viral, Animal ; diagnosis ; virology ; Interferon-gamma ; blood ; Interleukin-4 ; blood ; Male ; Medicine, Chinese Traditional ; Mice ; Mice, Inbred BALB C ; Murine hepatitis virus ; NF-kappa B p50 Subunit ; metabolism

<b>OBJECTIVEb>To investigate the effects of burn serum on nuclear translocation of monocytic NF-kappaB heterodimers p50/p65 and the degradation of inhibiting kappaB (IkappaBalpha), so as to further explore the role of burn serum on the activation of monocytes.

<b>METHODSb>Peripheral blood monocytes (PBMCs) isolated from healthy volunteers were employed as the target cells. The cells were stimulated by the serum from healthy volunteers and burn patients, and by burn serum together with pyrrolidine dithiocarbamate (PDTC). Sera from normal healthy volunteers were taken as control. The nuclear translocation of monocytic p50 and p65 at 30th, 60th, 120th and 480th post stimulation minutes (PSM) was observed with laser confocal microscopy. The degradation of monocytic IkappaBalpha protein at 30th, 60th, 90th and 120th PSM was determined by Western blot.

<b>RESULTSb>Compared to that in control group, the nuclear translocation of monocytic p50 and p65 took place 30 min after the PBMCs were stimulated by burn serum, peaking at 30 to 60 min, but it gradually recovered to pre-stimulation state at 2 hrs with decreased intra-nuclear collection. Meanwhile, the IkappaBalpha degradation occurred within 30 min after PBMCs being stimulated by burn serum, and it peaked at 60 mins. However, IkappaBalpha gradually reappeared in the cytoplasm after 2 hrs of stimulation. PDTC (an antioxidants) could effectively inhibit monocytic IkappaBalpha degradation and nuclear translocation of NF-kappaB induced by burn serum.

<b>CONCLUSIONb>Burn serum could induce nuclear translocation of p50 and p65 components of NF-kappaB in monocytes into the nucleus and degradation of IkappaBalpha, leading ultimately to the secretion of cytokines from the PBMCs.

Active Transport, Cell Nucleus ; Burns ; blood ; Cells, Cultured ; Female ; Humans ; I-kappa B Proteins ; metabolism ; Male ; Monocytes ; metabolism ; NF-KappaB Inhibitor alpha ; NF-kappa B p50 Subunit ; metabolism ; Transcription Factor RelA ; metabolism

<b>OBJECTIVEb>To investigate the effects of burn sera on the nuclear translocation of endothelial NF-kappaB heterodimers p50/p65 and on the degradation of inhibiting kappaB (IkappaBalpha), in order to explore the role of burn sera on activation of the endothelium.

<b>METHODSb>Cultured human umbilical vein endothelial cells (HUVECs) (ECV-304 strain) were employed as the target cells. The cells were stimulated by sera from healthy volunteers and from burn patients and burn sera together with PDTC (pyrrolidine dithiocarbarnate). The normal cultured cells were taken as the control. The nuclear translocation of endothelial p50/p65 at 30, 60, 120 and 480 mins after the stimulation was observed with laser confocal microscopy, and the endothelial IkappaBalpha protein degradation at 30, 60, 90 and 120 mins after the stimulation was determined by Western blotting.

<b>RESULTSb>When compared to that in control group, the nuclear translocation of p50/p65 took place 30 mins after the endothelial cells were stimulated by burn sera, and it reached the summit at 30 - 60 mins, but recovered to pre-stimulation state at 2hrs. In addition, IkBalpha degradation occurred 30 mins after the cells were stimulated by burn sera (P < 0.01) and peaking at 45 - 60 mins after the stimulation and recovered at 2hrs after the stimulation. The nuclear translocation of endothelial p50/p65 and IkBalpha degradation at 30 and 60 mins after the stimulation by burn sera could be effectively inhibited by PDTC.

<b>CONCLUSIONb>Burn sera might induce the nuclear translocation of endothelial NF-kappaB p50/p65 and IkappaBalpha degradation and activate NF-kappaB, which ultimately lead to the secretion of cytokines from the endothelium.

Active Transport, Cell Nucleus ; Adolescent ; Adult ; Burns ; blood ; Female ; Humans ; I-kappa B Proteins ; analysis ; Male ; Middle Aged ; NF-KappaB Inhibitor alpha ; NF-kappa B ; metabolism ; NF-kappa B p50 Subunit ; Transcription Factor RelA