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Biomedical subjects

Qi Luo

Publications and source records attributed to Qi Luo.

9 recordsLinked to original sources

[Diagnosis and treatment of concealed penis in 43 children].

OBJECTIVE: To improve the diagnosis and treatment of concealed penis in children. METHODS: From August 1998 to January 2004, 43 cases of concealed penis in children were treated with Huang Lugang's procedure aging aged 2-14 years (7 years on average). Eight children are obesity. The albuginea tissue were fixed to the lateral Buck's fascia at the base of the penis. Removal of the excessive suprapubic fat was given in 2 cases of obesity type. RESULTS: All patients were followed up from 3 to 24 months. The results were satisfactory in 35 (81.4%). The penile contour were dissatisfactory in 8 patients with obesity including 2 patients given removal of the excessive suprapubic fat. CONCLUSION: The Huang Lugang's procedure was simple and can achieved satisfactory results, but it should be used carefully in case of obesity type.

Adolescent↗

IL-13 acutely augments HIV-specific and recall responses from HIV-1-infected subjects in vitro by modulating monocytes.

We show in this study that acute exposure of PBMCs derived from HIV-infected subjects to IL-13 results in increased recall T cell lymphoproliferative responses against HIV-1 p24 (n = 30, p < 0.0001) and other recall Ags (influenza, n = 43, p < 0.0001; purified protein derivative tuberculin, n = 6, p = 0.0299). This effect is due to a mechanism that acutely targets APC function in the adherent monocyte subset, as shown by the expansion of CD4(+) T cell responses following coculture of IL-13-treated enriched CD14(+) monocytes with donor-matched enriched CD4(+) T cells and Ag. Exposure to IL-13 over 18-72 h resulted in a significant enhancement of monocyte endocytosis (n = 11, p = 0.0005), CD86 expression (n = 12, p = 0.001), and a significant decrease in spontaneous apoptosis (n = 8, p = 0.008). Moreover, IL-13 exposure induced a significant decrease of significantly elevated constitutive levels of PBMC-secreted TNF-alpha (n = 14, p < 0.001) and IL-10 (n = 29, p < 0.001) within 18 h of exposure ex vivo, also reflected by decreased gene expression in the adherent cell population. Our data show that IL-13 is able to acutely enhance the function of the CD14(+) cell subset toward supporting Ag-specific cell-mediated responses in chronic HIV-1 infection.

Adjuvants, Immunologic↗

Long-range detection and length estimation of light filaments using extra-attenuation of terawatt femtosecond laser pulses propagating in air.

High-energy femtosecond laser pulses propagating in the atmosphere undergo self-focusing resulting in the appearance of the phenomenon of filamentation. We observed an extra-attenuation of such (terawatt) femtosecond laser pulses propagating in the atmosphere when compared with long pulses (200 ps) with the same energy. This is because, in contrast to the linear propagation of the long pulse, the input femtosecond laser pulse is attenuated owing to either absorption through multiphoton ionization/tunnel ionization or to scattering on the laser-induced plasma; self-phase-modulation and self-steepening further convert partially the energy initially contained in the fundamental bandwidth into the broad side bands of the laser, becoming eventually a white-light laser pulse (supercontinuum). The experimental data allow us to extract an effective extra-attenuation coefficient for an exponential decay of the input pulse energy with the propagation distance. Such a coefficient allows us to estimate an upper bound of the filament length under the experimental conditions used. More generally, our observation leads to a new technique to remotely detect light filaments in the atmosphere.

Journal Article↗

Activation and repression of interleukin-12 p40 transcription by erythroid Kruppel-like factor in macrophages.

Transcription of interleukin (IL)-12 p40 in myeloid cells is attributed to the recruitment of multiple activated transcription factors such as nuclear factor kappaB (NFkappaB), CCAAT enhancer-binding protein beta, ets-2, PU.1, and so forth. We now provide the first description of the human erythroid Kruppel-like factor (EKLF) in human primary macrophages and identify the role of EKLF in IL-12 p40 expression. EKLF-specific binding to the CACCC element (-224 to -220) on the human IL-12 p40 promoter was observed in resting human primary macrophages. Functional analysis of the CACCC element revealed a dependent role for EKLF binding in activating IL-12 p40 transcription in resting RAW264.7 cells, whereas EKLF overexpression in the presence or absence of this element repressed IL-12 p40 transcription in interferon gamma/lipopolysaccharide-stimulated RAW264.7 cells. Murine endogenous IL-12 p40 mRNA was consistently induced by overexpressed EKLF in resting RAW264.7 cells, whereas EKLF suppressed IL-12 p40 expression in activated RAW264.7 cells. Modulation of nuclear binding activities at the IL-12 p40 NFkappaB half-site was induced by EKLF for down-regulation of IL-12 p40 transcription in activated RAW264.7 cells, but no effect of EKLF on NFkappaB activity was observed in resting RAW264.7 cells. Taken together, we identify EKLF as a transcription factor in macrophages able to regulate IL-12 p40 transcription depending on the cellular activation status. The bifunctional control of IL-12 p40 by EKLF and its modulation of NFkappaB support a potential function for this factor in orchestrating IL-12 p40 production in macrophages.

Animals↗

Autorepression of c-myc requires both initiator and E2F-binding site elements and cooperation with the p107 gene product.

Myc proteins are transcriptional activators, but also repress transcription through initiator (Inr) elements. Repression requires the conserved Myc Box II, but the cis-acting element(s) required for c-myc autorepression have eluded definition. Since the gene has a candidate Inr at the P2 promoter, we tested whether Myc autorepression operates through the Inr/BoxII mechanism. Overexpression of c-Myc but not a Box II deletion mutation represses both c-myc P2 reporter genes and endogenous c-myc, as does Mxi1 expression. Only 45 nucleotides surrounding the P2 start suffice to mediate autorepression, but Myc and Mxi1 also downregulate P2 Inr mutations, suggesting other core promoter sequence requirements for autorepression. We tested the importance of conserved E2F sites, based on known Myc interaction with the pRb-related p107 and on the transrepressive effects of Rb family proteins. Myc, Mxi1, and p107 repress c-myc somewhat less well in the absence of E2F binding sites, while an E2F+Inr double mutation is not repressed at all by these gene products. Further, Myc repression at the c-myc P2 core promoter is augmented by p107, but not by pRb or p130, nor by p107 lacking the conserved pocket domain. Our data suggest that Myc autorepression requires both the c-myc Inr and E2F sites in cis, as well as p107 in trans. Consistent with this, we found that retrovirally transduced c-Myc cannot downregulate endogenous c-myc in p107-null fibroblasts, and show evidence that both Myc and p107 are present in a complex assembled at the c-myc P2 core promoter.

Animals↗

HIV-1 transmission and cytokine-induced expression of DC-SIGN in human monocyte-derived macrophages.

Dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin (DC-SIGN) has been described as an attachment molecule for human immunodeficiency virus type 1 (HIV-1) with the potential to mediate its transmission. We examined DC-SIGN expression in monocyte-derived macrophages (MDM) and its role in viral transmission when MDM were exposed to interleukin (IL)-13, IL-4, or interferon-gamma (IFN-gamma). We show that IL-13 and IL-4 increase transcripts, total protein, and cell-surface expression of DC-SIGN in all MDM tested, IFN-gamma results ranged from no change to up-regulation of surface expression, and message and total protein were, respectively, induced in all and 86% of donors tested. Transmission experiments of HIV-1 X4 between cytokine-treated MDM to Sup-T1 cells showed no association between total transmission and DC-SIGN up-regulation. IL-4 but not IL-13 resulted in a less than twofold increase in MDM viral transmission to CD4+ T cells in spite of a fourfold up-regulation in DC-SIGN expression by either cytokine. In contrast, IFN-gamma treatment induced a decrease in total transmission by at least two-thirds, despite its induction of DC-SIGN. Soluble mannan resulted in a greater inhibition of viral transmission to CD4+ T cells than neutralizing anti-DC-SIGN monoclonal antibody (67-75% vs. 39-48%), supporting the role of mannose-binding receptors in viral transmission. Taken together, results show that DC-SIGN regulation in MDM does not singly predict the transmission potential of this cell type.

Acquired Immunodeficiency Syndrome↗

Therapeutic embolization of cavernous sinus dural arteriovenous fistulas via transvenous approach.

OBJECTIVE: To describe the transvenous catheterization technique for the treatment of cavernous sinus dural arteriovenous fistulas (CSdAVFs), including its indications, complications and efficacy. METHODS: Eight patients with symptomatic CSdAVFs were treated by endovascular embolization with platinum coils, via the inferior petrosal sinus (IPS) in 6 patients, and via the Sylvian vein after surgical exposure in other 2 patients. RESULTS: Complete angiographic resolution of the fistula was obtained in six patients immediately after the procedures, and a complete resolution of symptoms and signs was achieved in all patients. The residual fistulas in two patients disappeared completely in the follow-up angiography. CONCLUSION: Transvenous embolization is a useful and safe approach in the management of CSdAVFs.

Aged↗

Constitutive and induced expression of DC-SIGN on dendritic cell and macrophage subpopulations in situ and in vitro.

DC-SIGN is a C-type lectin, highly expressed on the surface of immature dendritic cells (DCs), that mediates efficient infection of T cells in trans by its ability to bind HIV-1, HIV-2, and SIV. In addition, the ability of DC-SIGN to bind adhesion molecules on surfaces of naïve T cells and endothelium also suggests its involvement in T-cell activation and DC trafficking. To gain further insights into the range of expression and potential functions of DC-SIGN, we performed a detailed analysis of DC-SIGN expression in adult and fetal tissues and also analyzed its regulated expression on cultured DCs and macrophages. First, we show that DC-SIGN expression is restricted to subsets of immature DCs in tissues and on specialized macrophages in the placenta and lung. There were no overt differences between DC-SIGN expression in adult and fetal tissues except that DC-SIGN expression in alveolar macrophages was only present after birth. Similarly, in tissues, DC-SIGN was observed primarily on immature (CD83-negative) DCs. Secondly, in the peripheral blood, we found expression of DC-SIGN on a small subset of BDCA-2+ plasmacytoid DC precursors (pDC2), concordant with our finding of large numbers of DC-SIGN-positive cells in allergic nasal polyps (previously shown to be infiltrated by DC2). Triple-label confocal microscopy indicated that DC-SIGN was colocalized with BDCA-2 and CD123 on DCs in nasal polyp tissue. Consistent with this finding is our observation that DC-SIGN can be up-regulated on monocyte-derived macrophages upon exposure to the Th2 cytokine, IL-13. In summary, our data demonstrate the relevant populations of DC and macrophages that express DC-SIGN in vivo where it may impact the efficiency of virus infection and indicate that DC-SIGN expression may be involved in the Th2 axis of immunity.

Adult↗