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Biomedical subjects

Xiang Li

Publications and source records attributed to Xiang Li.

At least 127 records · Page 7Linked to original sources

[The synergistic effects of docetaxol and retinoic acid on prostate cancer cell line PC-3].

OBJECTIVE: To observe the synergistic effects of docetaxol and retinoic acid on prostate cancer cell line PC-3 in vitro and in vivo. METHODS: Cell morphology, MTT, flow cytometry, immunocytochemical method were used to observe the effects of 10(-6) mol/L, 10(-7) mol/L, 10(-8) mol/L docetaxol and 10(-5) mol/L, 10(-6) mol/L, 10(-7) mol/L retinoic acid on prostate cancer cell line PC-3 in single or synergistic administration ways for 24 and 48 hours in vitro. Male BALB/C-nu mice with PC-3 prostate cancer cell lines were treated by docetaxol and retinoic acid singly or synergistically in vivo. Serum PSA of mice, weights of mice and PSA expression in xenograft tumors of mice by immunohistochemical method were measured. RESULTS: Above 10(-6) mol/L retinoic acid enhanced the growth suppression (suppression ratio > or = 69.2%, P<0.01), apoptosis (Apoptosis ratio > or = 23.8%, P<0.05) and down-regulation of the expression of cyclin D1 (expression ratio < or = 14.2%, P<0.05) induced by above 10(-7) mol/L docetaxol in PC-3 cells. Retinoic acid changed the ratio of G2/M phase induced by docetaxol from 70.3% to 54.6%, and reversed the G2/M arrest partially (P<0.05). Mean serum PSA of mice [(43+/-11) ng/ml], weight of xenograft tumors [(2.8+/-0.4) g] and PSA expression in tumors [(26+/-3.2)%] with PC-3 prostate cancer cell lines of nude mice were decreased significantly in docetaxol combined with retinoic acid group than in control group except weight of mice [(20.3+/-1.1) g]. CONCLUSION: Retinoic acid can enhance the growth suppression and apoptosis induced by docetaxol in synergistic way in vitro and in vivo, thus showing their great potential in the treatment of androgen-independent carcinoma of prostate.

Adult↗

[On the research of histone methylation].

The types of histone methyltransferases, the relationship between methylation of Lysine 9 of H3 and the formation of heterochromatin, gene regulation in euchromatin, and that with DNA methylation, were mainly introduced. The interrelation between histone methylation and histone acetylation/phosphorylation was summarized. It is showed that histone methylation plays a very important role in maintaining the balance state of cell. The future research tendency of histone methylation was fantastic.

Acetylation↗

[Measurement of tissue (correction of tissne) tension and ventilation resistance in eustachian (correction of eustachiam) tube opened by positive pressure in respiratory tract and the study on mechanism of ventilation].

OBJECTIVE: To determine the ventilation resistance of the Eustachian tube (VRET) and the lowest positive pressure to maintain the opening of the tube. Through which to elucidate the mechanism of positive ventilation. METHOD: To determine the tissue tension, 24 male flyers. Middle ear pressure was measured by a Zodiac 901 analyzer. To determine the VRET: when the Eustachian tube was opened, the change of pressure in the nasopharynx during the change of pressure in the external auditory canal was the VRET. In order to understand the relationship between middle ear barotraumas and VRET, 160 ears were tested in flight, and 60 ears were tested in the hypobaric chamber. RESULT: The Eustachian tube ventilation resistance was found to have a large respective divergence (1.20-6.86 kPa). When the tube was opened, the pressure of the middle ear changed with the change of the mask pressure. When the mask pressure dropped to 0.70 kPa, the middle ear pressure dropped down to 0 kPa. The individual difference was comparatively small. Among 160 ears of 80 combat aircraft flyers in flight, 19 ears had presentations of middle ear barotalgia. 141 ears had no presentation of barotalgia. The VRET's were significantly different (P<0.001). Among the 60 ears of 30 flyers tested in the low-pressure chamber, 9 ears had presentations of middle ear barotraumas. 51 ears had no presentation of barotalgia. The difference between the VRET's were also significant (P<0.001). CONCLUSION: If there is enough positive pressure in the mask, it will open the Eustachian tube. Then, it needs only a small positive pressure (about 0.70 kPa) to maintain the tube open. The airflow in the tube follows the law of pneumatics. The occurrence of barotalgia and VRET are correlative.

Adult↗

Critical role of CXC chemokines in endotoxemic liver injury in mice.

Tissue accumulation of leukocytes constitutes a rate-limiting step in endotoxin-induced tissue injury. Chemokines have the capacity to regulate leukocyte trafficking. However, the role of CXC chemokines, i.e., macrophage inflammatory protein-2 (MIP-2) and cytokine-induced neutrophil chemoattractant (KC), in leukocyte recruitment, microvascular perfusion failure, cellular injury, and apoptosis in the liver remains elusive. Herein, mice were challenged with lipopolysaccharide (LPS) in combination with D-galactosamine, and intravital microscopy of the liver microcirculation was conducted 6 h later. It was found that immunoneutralization of MIP-2 and KC did not reduce LPS-induced leukocyte rolling and adhesion in postsinusoidal venules. In contrast, pretreatment with monoclonal antibodies against MIP-2 and KC abolished (83% reduction) extravascular recruitment of leukocytes in the livers of endotoxemic mice. Notably, endotoxin challenge increased the expression of CXC chemokines, which was mainly confined to hepatocytes. Moreover, endotoxin-induced increases of liver enzymes and hepatocellular apoptosis were decreased by more than 82% and 68%, respectively, and sinusoidal perfusion was restored in mice passively immunized against MIP-2 and KC. In conclusion, this study indicates that intravascular accumulation of leukocytes in the liver is independent of CXC chemokines in endotoxemic mice. Instead, our novel data suggest that CXC chemokines are instrumental in regulating endotoxin-induced transmigration and extravascular tissue accumulation of leukocytes. Indeed, these findings demonstrate that interference with MIP-2 and KC functions protects against septic liver damage and may constitute a potential therapeutic strategy to control pathological inflammation in endotoxemia.

Animals↗

Simplicial edge representation of protein structures and alpha contact potential with confidence measure.

Protein representation and potential function are two important ingredients for studying protein folding, equilibrium thermodynamics, and sequence design. We introduce a novel geometric representation of protein contact interactions using the edge simplices from the alpha shape of the protein structure. This representation can eliminate implausible neighbors that are not in physical contact, and can avoid spurious contact between two residues when a third residue is between them. We developed statistical alpha contact potential using an odds-ratio model. A studentized bootstrap method was then introduced to assess the 95% confidence intervals for each of the 210 propensity parameters. We found, with confidence, that there is significant long-range propensity (>30 residues apart) for hydrophobic interactions. We tested alpha contact potential for native structure discrimination using several sets of decoy structures, and found that it often performs comparably with atom-based potentials requiring many more parameters. We also show that accurate geometric representation is important, and that alpha contact potential has better performance than potential defined by cutoff distance between geometric centers of side chains. Hierarchical clustering of alpha contact potentials reveals natural grouping of residues. To explore the relationship between shape and physicochemical representations, we tested the minimum alphabet size necessary for native structure discrimination. We found that there is no significant difference in performance of discrimination when alphabet size varies from 7 to 20, if geometry is represented accurately by alpha simplicial edges. This result suggests that the geometry of packing plays an important role, but the specific residue types are often interchangeable.

Amino Acid Sequence↗

Use of Hsf1(-/-) mice reveals an essential role for HSF1 to protect lung against cadmium-induced injury.

Cadmium (Cd) is known to activate heat shock (HS) response, which is characterized by overexpression of heat shock proteins (Hsps) under the control of heat shock factor 1 (HSF1). The potential protection provided by the HS response, induced by increasing the body temperature of animals before Cd exposure or by Cd itself, against pathophysiological changes occurring after Cd intranasal instillation (1 to 100 microg/mouse) was examined. HSF1-deficient mice were used to evaluate the role of this factor in lung protection. Cd instillation caused dose- and time-dependent changes in the respiratory pattern measured by plethysmography (Penh), and significant increases in lactate dehydrogenase (LDH) activity as well as macrophage and neutrophil counts in bronchoalveolar lavage fluids. HS preconditioning induced Hsp overexpression and reduced the Penh (-30%), LDH (-25%), and neutrophil (-55%) responses to subsequent administration of the highest Cd doses (50 and 100 microg) in wild-type mice. HSF1 deficiency abolished the HS response and its protective effect. In the absence of preconditioning, Hsf1(-/-) mice exhibited higher values of Penh (+70%) and LDH activity (+42%) compared with wild-type animals when exposed to the lowest Cd doses. Higher macrophage (+80%) and neutrophil counts (+115%) were recorded whatever the dose. Western blot analyses indicated that lung protection might be related to the kinetics of HSF1-dependent Hsp70 expression. Altogether, our data demonstrate that HS response elicited both by prior HS and by Cd itself moderates pulmonary injuries due to Cd instillation, and that HSF1 is a major mediator in this protection.

Animals↗

Up-regulation of secretory leukocyte protease inhibitor (SLPI) in the brain after ischemic stroke: adenoviral expression of SLPI protects brain from ischemic injury.

Secretory leukocyte protease inhibitor (SLPI) is a 12-kDa secreted protein initially identified from epithelial cells as an inhibitor of leukocyte serine proteases. In the present study, we described the identification of SLPI expression in ischemic cortex by suppression subtractive hybridization strategy. Our full-length rat SLPI cDNA shares 81% and 63% amino acid sequence identity with its mouse and human homologs, respectively, and with several polymorphisms to previous reported rat sequences. Northern blot analysis confirmed that SLPI mRNA was significantly induced in the ischemic brain tissue at 12 h (5.1-fold increase over sham controls, n = 4, p < 0.05), peaked at 2 days (26.1-fold increase, p < 0.001), and sustained up to 5 days (5.1-fold increase, p < 0.05). SLPI was localized in neurons and astrocytes in the peri-infarct zone from 24 to 72 h after middle cerebral artery occlusion by means of immunohistochemical and confocal microscopy analysis. Administration of a recombinant adenovirus overexpressing SLPI (Adv/SLPI) into the cortical tissue resulted in up to 58.4% reduction in ischemic lesion over controls at the site of Adv/SLPI expression (p < 0.01, n = 8) and significantly improved functional outcome (p < 0.01). These data suggest that the ischemia-induced expression of SLPI might play a neuroprotective role in focal stroke, possibly because of rapid inhibition of activated proteases and its suppression in inflammatory response.

Adenoviridae↗

[Rapid identification of Cortex moutan radicis and similar aromatic Chinese herbs by headspace gas chromatography].

OBJECTIVE: To establish the method for rapid identification of the quality of Cortex moutan radicis and similar aromatic Chinese herbs by headspace gas chromatography (HSGC). METHODS: The constituents of headspace gas from Chinese herbs, such as Cortex moutan radicis,Radix cynanchi paniculati and root-bark of Paeonia lactiflora. were analyzed by HSGC. RESULTS: The characteristic finger-print headspace chromatograms of these three drugs were different from one another. Cortex moutan radicis stored for 4 years under common conditions contained only traces of paeonol. CONCLUSION: HSGC was simple, quick and accurate in identifying and controlling the quality of aromatic Chinese herbs.

Acetophenones↗

[Clinical study of sildenafil in the treatment of premature ejaculation complicated by erectile dysfunction].

OBJECTIVES: To evaluate the efficacy and safety of sildenafil citrate in the treatment of premature ejaculation (PE) complicated by erectile dysfunction (ED). METHODS: Forty-five patients of PE complicated by ED received flexible doses of sildenafil from 50 to 100 mg for 1 to 3 months. Intravaginal ejaculatory latency time (IELT) and sexual satisfaction ratio (SSR) of partner were recorded to evaluate the effect of PE treatment, as well as the general efficacy and satisfaction of ED treatment. And the difference of IIEF-5 before and after the treatment were compared. RESULTS: Twenty-seven patients had their PE improved and the effective rate was 60%. Forty patients reported the improvement in erection and the percentage of erectile improvement was 88.88%. All the 27 patients with improvement of PE achieved effective erection through the administration of 50 mg sildenafil and the satisfaction rate reached 81.48%. On the other hand, only 1 case (5.56%) reported satisfaction over the treatment in the 18 patients who did not obtain improvement of PE. Between the PE improvement group and non-improvement group, there were significant differences (P < 0.001) shown in IIEF-5 scores before and after the treatment. Mild or moderate side effects were reported in 9 patients(20%), who recovered without any treatment. CONCLUSIONS: To premature ejaculation patients with ED, sildenafil can safely and effectively improve their erectile function, the satisfaction over the ED treatment outcome means that their PE symptoms could be alleviated.

Adult↗

IKKalpha, IKKbeta, and NEMO/IKKgamma are each required for the NF-kappa B-mediated inflammatory response program.

The IKKbeta and NEMO/IKKgamma subunits of the NF-kappaB-activating signalsome complex are known to be essential for activating NF-kappaB by inflammatory and other stress-like stimuli. However, the IKKalpha subunit is believed to be dispensable for the latter responses and instead functions as an in vivo mediator of other novel NF-kappaB-dependent and -independent functions. In contrast to this generally accepted view of IKKalpha's physiological functions, we demonstrate in mouse embryonic fibroblasts (MEFs) that, akin to IKKbeta and NEMO/IKKgamma, IKKalpha is also a global regulator of tumor necrosis factor alpha- and IL-1-responsive IKK signalsome-dependent target genes including many known NF-kappaB targets such as serum amyloid A3, C3, interleukin (IL)-6, IL-11, IL-1 receptor antagonist, vascular endothelial growth factor, Ptx3, beta(2)-microglobulin, IL-1alpha, Mcp-1 and -3, RANTES (regulated on activation normal T cell expressed and secreted), Fas antigen, Jun-B, c-Fos, macrophage colony-stimulating factor, and granulocyte-macrophage colony-stimulating factor. Only a small number of NF-kappaB-dependent target genes were preferentially dependent on IKKalpha or IKKbeta. Constitutive expression of a trans-dominant IkappaBalpha superrepressor (IkappaBalphaSR) in wild type MEFs confirmed that these signalsome-dependent target genes were also dependent on NF-kappaB. A subset of NF-kappaB target genes were IKK-dependent in the absence of exogenous stimuli, suggesting that the signalsome was also required to regulate basal levels of activated NF-kappaB in established MEFs. Overall, a sizable number of novel NF-kappaB/IKK-dependent genes were identified including Secreted Frizzled, cadherin 13, protocadherin 7, CCAAT/enhancer-binding protein-beta and -delta, osteoprotegerin, FOXC2 and FOXF2, BMP-2, p75 neurotrophin receptor, caspase-11, guanylate-binding proteins 1 and 2, ApoJ/clusterin, interferon (alpha and beta) receptor 2, decorin, osteoglycin, epiregulin, proliferins 2 and 3, stromal cell-derived factor, and cathepsins B, F, and Z. SOCS-3, a negative effector of STAT3 signaling, was found to be an NF-kappaB/IKK-induced gene, suggesting that IKK-mediated NF-kappaB activation can coordinately illicit negative effects on STAT signaling.

Animals↗

[Inhibitory effect of alveolar macrophages on the proliferation of pulmonary fibroblasts].

The effect of alveolar macrophages (AM) harvested from Wistar rats by lung lavage on proliferation of human embryo pulmonary fibroblasts in culture was investigated. It was observed that supernatants of AM decreased the uptake of (3)H TdR by the pulmonary fibroblasts. The AM activated with opsonized zymosan (OPZ) showed a stronger inhibitory effect on fibroblast proliferation compared with inactivated AM. Following pretreatment with indomethacin, the inhibitory effect of AM was abolished and reversed to stimulatory effect on pulmonary fibroblast proliferation. The PGE content in AM supernatant was measured with radioimmunoassay. It was observed that the inhibitory effect of AM was highly correlated to prostaglandin (PGE) content in the supernatant of AM. The results suggest that AM has both inhibitory and stimulatory effects on the proliferation of pulmonary fibroblast; the inhibitory effect is primary under normal conditions. This inhibitory action is mainly due to PGE secreted from AM. It is, therefore, suggested that AM plays an important role in suppressing pulmonary fibrosis under normal conditions.

Animals↗

Human prostate cancer cell death by novel anticancer compounds, apoptosis-inducing nucleosides from CD57+ HLA-DR(bright) natural suppressor cell line.

BACKGROUND: We validated the induction of apoptosis in human prostate cancer PC3 cells by apoptosis-inducing nucleosides (AINs) released from the CD57(+)HLA-DR(bright)-natural suppressor (57.DR-NS) cell line. We analyzed the molecular signaling pathway during AINs-induced apoptosis in PC3 cells. METHODS: Direct and indirect co-cultures between 57.DR-NS and PC3 cells were performed. AINs were isolated by high-performance liquid chromatography (HPLC) from 57.DR-NS cell cultures. Apoptosis in PC3 cells was analyzed by DNA fragmentation, sub-G(1) DNA content with flow cytometry, and terminal deoxynucleotide transferase-mediated dUTP nick end-labeling (TUNEL) method. The DNA strand breaks and activation of caspase-3 in PC3 cells were measured by DNA unwinding and flow cytometry assay. RESULTS: The 57.DR-NS cell line generated apoptosis in PC3 cells via AINs. AINs isolated from 57.DR-NS cell cultures induced apoptosis in PC3 cells. Furthermore, we found DNA strand breaks followed by activation of caspase-3 during AINs-induced apoptosis in PC3 cells. CONCLUSIONS: The data obtained here indicated that AINs could induce apoptosis in PC3 cells through DNA strand breaks and activation of caspase-3.

Apoptosis↗

NKX-3.1 interacts with prostate-derived Ets factor and regulates the activity of the PSA promoter.

The NKX-3.1 homeobox gene maps to human chromosome 8p21, a region that undergoes frequent loss of heterozygosity in prostate tumors. Loss of Nkx-3.1 function in mice leads to epithelial overgrowth. To further elucidate the molecular basis of NKX-3.1 function, a genetic screen for proteins that interact with NKX-3.1 was performed. Prostate-derived Ets factor (PDEF) was identified as a potential partner of NKX-3.1. Coimmunoprecipitation analyses demonstrated that NKX-3.1 and PDEF are physically associated in prostate epithelial cells. Cotransfection analyses demonstrated that NKX-3.1 can abolish the transcriptional activation function of PDEF on the prostate-specific antigen (PSA) promoter. These data identify PSA as a target gene for NKX-3.1 and provide new insights into the function of this candidate tumor suppressor.

Epithelial Cells↗

Human malignant cell death by apoptosis-inducing nucleosides from the decidua derived CD57(+)HLA-DR(bright) natural suppressor cell line.

The CD57(+)HLA-DR(bright) natural suppressor (57.DR-NS) cell line derived from human decidual tissue mediated apoptosis of human leukemia Molt4 and carcinoma BeWo/GCIY cells but not human fibroblast WI-38 cells, and apoptosis-inducing nucleosides (AINs) appeared to be involved. Six AINs were released into 57.DR-NS cell culture media and were isolated by the combination of physicochemical procedures of C18 preparative column, thin layer chromatography (TLC) and high pressure liquid chromatography (HPLC). Subsequently, we demonstrated that AINs could induce apoptosis in the human malignant Molt4/BeWo/GCIY cell line but not human normal WI-38 fibroblasts. Apoptosis was characterized by DNA strand breaks and activation of the caspase cascade, especially caspase-3. The administration of AINs into GCIY tumor bearing SCID mice culminated in suppression of tumor growth due to apoptosis of tumor cells.

Animals↗

Induction of apoptosis mediated by fas receptor and activation of caspase-3 in MRL-+/+ or MRL-lpr/lpr murine oocytes.

The molecular mechanisms leading to ovarian follicular atresia in the typical pathways of programmed cell death remain to be clarified. Here we have demonstrated that the apoptotic signalling pathway in MRL-+/+ (MRL/+) murine oocytes is through the Fas receptor followed by the activation of caspase-3. In contrast, we found that the aberrant expression and dysfunction of the mutant Fas receptor in MRL-lpr/lpr (MRL/lpr) murine oocytes caused by insertion of the early transposable element (ETn) into the Fas gene were associated with an inability to activate the caspase cascade (especially caspase-3) and to induce nuclear DNA fragmentation. These findings indicate that the induction of apoptosis in MRL/lpr murine oocytes did not occur in the presence of a defective Fas receptor lacking the death domain to trigger the caspase cascade, suggesting a failure to induce ovarian follicular atresia.

Animals↗

B cells express Ly-6C in a Th1 but not Th2 cytokine environment.

Interferon-alpha (IFN-alpha) is the primary regulator of transient Ly-6C expression on T cells. B cells, which do not express Ly-6C in the resting state, have been reported to express Ly-6C following exposure to proinflammatory stimuli. This study examined the factors controlling Ly-6C expression on B cells and the kinetics of Ly-6C expression in the presence of these factors. In vivo studies demonstrated that proinflammatory (Th1) cytokines transiently upregulate B cell Ly-6C expression. In vitro studies identified Th1 cytokines, particularly IFN-alpha and IFN-gamma, as the principal cytokines responsible for this induction. Polyclonal B cell activators (anti-IgM and recombinant CD40 ligand trimer) showed minimal ability to independently induce Ly-6C expression on B cells but did enhance the ability of IFNs to induce expression. Th2 cytokine environments did not result in B cell Ly-6C expression, and interleukin-4 (IL-4) actually antagonized the IFN-driven induction of Ly-6C. Ly6.1 strains of mice consistently demonstrated a greater ability to express Ly-6C on B cells than did Ly-6.2 strains. Together, these studies demonstrate the ability of Th1 but not Th2 cytokine environments to transiently induce the expression of Ly-6C on B cells and provide additional evidence for differences in the regulation of Ly-6C expression in Ly6.1 and Ly6.2 strains.

Animals↗

Magnetic resonance urography in the diagnosis of urinary tract obstruction after renal transplantation.

OBJECTIVE: To evaluate magnetic resonance urography (MRU) in the diagnosis of urinary tract obstruction after renal transplantation. METHODS: A total of 31 patients with suspected urinary tract obstruction after renal transplantation were examined, and the results were compared with those from surgery and B-ultrasound examination. RESULTS: The urinary tract after renal transplantation was clearly shown using MRU, and all patients were clearly diagnosed by MRU. Imaging results were consistent with those from surgery. CONCLUSIONS: MRU is suitable for detecting urinary tract obstruction after renal transplantation. It is a alternative method for IVP and CT in patients with renal function impairment and uremia.

Humans↗