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S Qin

Publications and source records attributed to S Qin.

At least 91 records · Page 5Linked to original sources

T-lymphocytes regulate genetically determined airway hyperresponsiveness in mice.

Airway hyperresponsiveness (AHR) is a hallmark of asthma and a heritable polygenic trait in the mouse. In the mouse, candidate gene products of hematopoietic origin implicated in asthma mapped to the regions of the previously defined quantitative trait loci. Since hematopoietic cells have been implicated in the pathogenesis of asthma, we evaluated the role of hematopoietic cells in general and T cells specifically in the genetic modulation of native airway responsiveness in mice. Here, with the use of bone marrow transplantation, anti-T-cell monoclonal antibody treatment and T-cell transfer, we demonstrate that intrinsic non-atopic AHR is mediated by T lymphocytes. Our data support the novel concept that, in the absence of identified environmental influences, T cells enhance genetically determined airway responsiveness.

Adoptive Transfer↗

Reduction of allergic airway responses in P-selectin-deficient mice.

P-selectin is an adhesion receptor that has been shown to be important in the recruitment of eosinophils and lymphocytes in a variety of inflammatory conditions. Because cellular recruitment is thought to be a critical event in allergen-induced changes in airway responsiveness, we reasoned that P-selectin-deficient mice would exhibit reduced airway responsiveness and cellular trafficking noted in wild-type (+/+) mice. Both (+/+) and P-selectin-deficient (-/-) mice sensitized and challenged with ovalbumin (OVA/OVA) exhibited the same capacity to produce increased titers of total and OVA-specific immunoglobulin E. Airway responsiveness to methacholine was significantly greater in the (+/+) (OVA/OVA) animals than it was in the respective (-/-) (OVA/OVA) group or control groups (P = 0.0016). Bronchoalveolar lavage fluid from (-/-) (OVA/OVA) mice contained significantly fewer eosinophils and lymphocytes compared with the (+/+) (OVA/OVA) mice (P < 0.05). These results suggest that the predominant role of P-selectin in OVA-induced airway hyperresponsiveness is to promote the airway inflammatory response to allergen inhalation.

Airway Resistance↗

Infiltration of eosinophils into the asthmatic airways caused by interleukin 5.

Interleukin (IL)-5 is thought to play an important role in asthmatic bronchial mucosal inflammation and is a potential therapeutic target. To investigate the effect of IL-5 on the infiltration of eosinophils in airway in vivo, we compared eosinophil counts and their activation status in airways without and after the topical instillation of recombinant human IL-5. Eight subjects with mild atopic asthma underwent initial bronchoscopy during which control bronchoalveolar lavage (BAL) fluid as well as bronchial mucosa were obtained, and at the same time, normal saline and IL-5 were administered to two sublobar segments separately. The second bronchoscopy were carried out and samples from challenged sites were taken 24 h later. It was found that the total eosinophils (BMK-13+ cells) and the activated eosinophils (EG2+ cells) in bronchial mucosa, the eosinophil numbers in BAL fluid, as well as eosinophil cationic protein (ECP) in BAL fluid from saline-challenged segments were not different from those in unchallenged segments. However, a significant eosinophilia was observed in bronchial mucosa and BAL fluid from IL-5-challenged sites. Eosinophil activation, as assessed by secretion of ECP, was also increased significantly in bronchial mucosa and BAL fluid. The results strongly suggested that IL-5 is capable of inducing eosinophil infiltration into the asthmatic airways, as well as the activation of infiltrating eosinophils.

Adult↗

[Optimal high-yield agronomic measures for Curcuma longa L].

Regression method of orthogonal conic substitution with factors was employed to build up a tuber yield simulation model. Three main measures (sowing time, plant population, application rate of fertilizer) affecting the tuber yield were analyzed by the mathematical model of three unknown second order orthogonal rotative regression. The optimal agronomic measures were obtained. The results indicate that sowing time and plant population play a important role in raising the tuber yield. Sowing time is clearly interrelated with plant population, and likewise, plant population application rate of fertilizer.

Fertilizers↗

[Effect of cultivating measures on the tuber yield of Curcuma longa L].

The effect of cultivating measures on the tuber yield of Curcuma longa was observed. dibble planting has been proved move effective in raising the tuber yield than drill culture, and the dibble planting quantity has no effect on the tuber. The rational producing area, soil, seed tuber and so on were selected according to the experiments.

Methods↗

[Ontogeny of Curcuma longa L].

Based on the research of growth of organs, accumulation of dry matter, distribution of photosynthetic production and displacement of growth centre, the growth of turmeric can be divided into three stages. There are 13 leaves in the life of turmeric. Leaf formation takes place rapidly to form 8 leaves in the seedling stage. The leaf area and increase of dry matter per day in roots and leaves are smaller or lower in the seedling stage. In the daughter rhizome formation stage, NAR reaches the maximum (3.54/m2.d), and the leaf area reaches the maximum(3302.9 cm2/plant, LAI 4.95). Before the daughter rhizome formation stage, more than 75% of dry matters are distributed in leaves, and in the daughter rhizome formation stage, 50%-75% of dry matters are distrbuted in leaves. In the late growing period, more than 40% of dry matters are distributed in the daughter rhizome. The growth centre of turmeric changes two times in life. When CGRr is equal to CGRt, the crossing of CGRt and CGRr curves may be regarded as the evidence of the transfer of growth centre from leaves to daughter rhizome.

Pharmacognosy↗

Evidence of increased endogenous carbon monoxide production in newborn rat endotoxicosis.

Carbon monoxide is thought to serve as a new endogenous mediator in the pathogenesis of sepsis and septic shock. In newborn rat endotoxicosis, carbon monoxide levels in the circulation as well as liver, kidney and lung were found to be significantly increased (P < 0.05). Moreover, the elevations of carbon monoxide correlated with enhanced nitric oxide production as indicated by nitrite/nitrate levels (P < 0.05). Our present data showed for the first time that endogenously produced carbon monoxide was increased during the course of shock-like states, which suggested that the role of carbon monoxide in sepsis and septic shock might worth further study.

Animals↗

[Effect of heat, noise and their combination on plasma and myocardial angiotensin II in rats].

Effects of heat (40 degrees C, relative humidity 82%), noise (115dB) and the combination of heat and noise on angiotensin (A II) content in plasma and myocardia was observed in rats. The results showed: (1) plasma A II in control group, heat group, noise group and combined group were 358.72 +/- 35.78, 624.08 +/- 36.32, 783.27 +/- 34.32 and 619.65 +/- 37.72 pg/ml respectively. The A II content in heat group, noise group and combined group are significantly higher than that of the control group (P<0.01). The increase in noise group was significant as compared with those in the heat group and combined group (P<0.05). (2) The myocardia A II in control group, heat group, noise group and combined group were 594.78 +/- 82.46, 935.10 +/- 15l.51, 326.22 +/- 28.45, and 438.37 +/- 58.63 pg/mg W.W respectively. The myocardial A II content in heat group was significantly higher (P<0.01), but that in noise group than the control was significantly lower(P<0.O5).

Angiotensin II↗

Interleukin-8 receptor B immunoreactivity in brain and neuritic plaques of Alzheimer's disease.

Cytokines mediate inflammatory responses through their receptors in the hematopoietic system. In a search for potential mediators of inflammatory responses in Alzheimer's disease, we examined brain for cytokine receptors. Herein we describe interleukin-8 receptor B (IL-8RB, also termed CXCR2) immunoreactivity in the central nervous system. Strong IL-8RB immunoreactivity is present in both Alzheimer's disease and control brains. Neurons, dendrites, and axons are clearly immunoreactive. In Alzheimer's disease, IL-8RB immunoreactivity is also present in some swollen dystrophic neurites of neuritic plaques. Double staining and confocal microscopic analysis reveals that these IL-8RB-positive neurites in plaques are neurofilament positive and are distinct from astrocytic or microglial processes. In general, these IL-8RB-positive neurities do not co-localize with PHF-1 or AT8 (hyperphosphorylated tau) immunoreactive neurites but instead co-localize with beta PP-positive neurites. These results demonstrate for the first time IL-8RB immunoreactivity in the central nervous system and imply a new role for this receptor outside the hematopoietic system. The strong presence of IL-8RB on neurons and the potential of glial cells to produce IL-8 suggest that this system might mediate neuronal-glial interactions.

Adult↗

Discrete steps in binding and signaling of interleukin-8 with its receptor.

The mechanisms by which chemokines bind and signal through their receptors are complex and poorly understood. In the present study, we sought to dissect these processes and to map important functional domains of the two CXC chemokine (interleukin-8) receptors, CXCR1 (formally IL-8RA) and CXCR2 (formally IL-8RB), using blocking monoclonal antibodies (mAbs) to the receptors and a series of chimeras between CXCR1 and CXCR2. A panel of specific mAbs against CXCR1 or CXCR2, generated by immunizing mice with transfectants expressing either receptor, were shown to effectively block IL-8- and/or growth-related oncogene alpha (GROalpha) -mediated ligand binding, chemotaxis, elastase release, and VCAM-1 binding in CXCR1 and CXCR2 transfectants and/or human neutrophils. Of particular interest was an anti-CXCR1 mAb, 7D9, that inhibited chemotaxis, elastase release, and VCAM-1 binding but had no detectable effects on ligand binding. The epitopes of these blocking mAbs were mapped by using a series of CXCR1/2 chimera transfectants and synthetic peptides. Most of the anti-CXCR1 antibodies, except 7D9, mapped to the amino acid sequence WDFDDL (CXCR1 residues 10-15), and all the anti-CXCR2 antibodies mapped to the amino acid sequence FEDFW (CXCR2 residues 6-10). The epitope of mAb 7D9 mainly involved a region within the first 45 residues of CXCR1, and it appeared to be conformation-sensitive. These results support a model in which the binding and signaling of IL-8 with its receptor occur in at least two discrete steps involving distinct domains of the receptor. This model is consistent with the notion that discrete conformational changes of the receptor secondary to ligand binding are required to trigger various biological responses. Moreover, the ligand binding and chemotaxis properties of each CXCR1/2 chimeric receptor to IL-8 and GROalpha were determined. It was found that each is distinct in its ability to confer ligand binding and chemotactic response to IL-8 and GROalpha, and two conclusions could be made. 1) The N-terminal segment of CXCR1 is a dominant determinant of receptor subtype selectivity, consistent with previous studies using rabbit/human CXCR1/2 chimeras; and 2) the specificity determinant for GROalpha binding in CXCR2 involves sequences in the N terminus, distal to the first 15 residues, as well as other parts of the receptor.

Amino Acid Sequence↗

Different functions for the interleukin 8 receptors (IL-8R) of human neutrophil leukocytes: NADPH oxidase and phospholipase D are activated through IL-8R1 but not IL-8R2.

Two monoclonal antibodies, anti-IL8R1 and anti-IL8R2, raised against both interleukin 8 receptors (IL-8R) of human neutrophils, IL-8R1 and IL-8R2, were used to study individual receptor functions after stimulation with IL-8, GRO alpha, or NAP-2. Efficacy and selectivity of the antibodies were tested in Jurkat cells transfected with cDNA coding for one or the other receptor. The binding of 125 I labeled IL-8 and IL-8-induced changes of the cytosolic free Ca2+ concentration were inhibited by anti-IL8RI in cells expressing IL-8R1 and by anti-IL8R2 in cells expressing IL-8R2. In human neutrophils, release of elastase was observed after stimulation with IL-8 or GRO alpha. The response to IL-8 was inhibited slightly by anti-IL8R1 and more substantially when both monoclonal antibodies were present, while the response to GRO alpha was inhibited by anti-IL8R2 but was not affected by anti-IL8R1. These results indicate that both IL-8 receptors can signal independently for granule enzyme release. Superoxide production, a measure of the respiratory burst, was obtained with increasing concentrations of IL-8 with maximum effects at 25 to 50 nM, but no response was observed upon challenge with GRO alpha or NAP-2 up to 1000 nM. The superoxide production induced by IL-8 was inhibited by anti-IL8R1, but was not affected by anti-IL8R2. Stimulation of neutrophils with IL-8, in contrast to GRO alpha or NAP-2, also elicited phospholipase D activity. The effect of IL-8 was again inhibited by anti-IL-8R1 but not by anti-IL8R2, indicating that this response, like the respiratory burst, was mediated by IL-8R1. Taken together, our results show that IL-8R1 and IL-8R2 are functionally different. Responses, such as cytosolic free Ca2+ changes and the release of granule enzymes, are mediated through both receptors, whereas the respiratory burst and the activation of phospholipase D depend exclusively on stimulation through IL-8R1.

Antigens, CD↗

Molecular cloning and characterization of a human eotaxin receptor expressed selectively on eosinophils.

The chemokine eotaxin is unusual in that it appears to be a highly specific chemoattractant for eosinophils. Ligand-binding studies with radiolabeled eotaxin demonstrated a receptor on eosinophils distinct from the known chemokine receptors CKR-1 and -2. The distinct eotaxin binding site on human eosinophils also bound RANTES (regulated on activation T expressed and secreted) and monocyte chemotactic protein (MCP)3. We have now isolated a cDNA from eosinophils, termed CKR-3, with significant sequence similarity to other well characterized chemokine receptors. Cells transfected with CKR-3 cDNA bound radiolabeled eotaxin specifically and with high affinity, comparable to the binding affinity observed with eosinophils. This receptor also bound RANTES and MCP-3 with high affinity, but not other CC or CXC chemokines. Furthermore, receptor transfectants generated in a murine B cell lymphoma cell line migrated in transwell chemotaxis assays to eotaxin, RANTES, and MCP-3, but not to any other chemokines. A monoclonal antibody recognizing CKR-3 was used to show that eosinophils, but not other leukocyte types, expressed this receptor. This pattern of expression was confirmed by Northern blot with RNA from highly purified leukocyte subsets. The restricted expression of CKR-3 on eosinophils and the fidelity of eotaxin binding to CKR-3, provides a potential mechanism for the selective recruitment and migration of eosinophils within tissues.

Amino Acid Sequence↗

A high-resolution physical map of human chromosome 11.

The development of a highly reliable physical map with landmark sites spaced an average of 100 kbp apart has been a central goal of the Human Genome Project. We have approached the physical mapping of human chromosome 11 with this goal as a primary target. We have focused on strategies that would utilize yeast artificial chromosome (YAC) technology, thus permitting long-range coverage of hundreds of kilobases of genomic DNA, yet we sought to minimize the ambiguities inherent in the use of this technology, particularly the occurrence of chimeric genomic DNA clones. This was achieved through the development of a chromosome 11-specific YAC library from a human somatic cell hybrid line that has retained chromosome 11 as its sole human component. To maximize the efficiency of YAC contig assembly and extension, we have employed an Alu-PCR-based hybridization screening system. This system eliminates many of the more costly and time-consuming steps associated with sequence tagged site content mapping such as sequencing, primer production, and hierarchical screening, resulting in greater efficiency with increased throughput and reduced cost. Using these approaches, we have achieved YAC coverage for >90% of human chromosome 11, with an average intermarker distance of <100 kbp. Cytogenetic localization has been determined for each contig by fluorescent in situ hybridization and/or sequence tagged site content. The YAC contigs that we have generated should provide a robust framework to move forward to sequence-ready templates for the sequencing efforts of the Human Genome Project as well as more focused positional cloning on chromosome 11.

Chimera↗

Cooperation of tyrosine kinases p72syk and p53/56lyn regulates calcium mobilization in chicken B cell oxidant stress signaling.

A chicken B cell line DT40 and its syk-negative or lyn-negative mutants were used to investigate the roles of protein-tyrosine kinases in oxidant stress signaling. The data presented here for wild-type cells demonstrate that hydrogen peroxide stimulates p53/56lyn-dependent tyrosine phosphorylation and activation of p72syk, and induces a rapid and prolonged elevation of intracellular calcium, which consists of calcium release from intracellular stores and influx from the extracellular space. Hydrogen-peroxide-triggered calcium mobilization was impaired in both syk-negative and lyn-negative cells, which was mainly due to the loss of calcium release from intracellular stores. Further studies indicated that inositol trisphosphate production was also abolished in both syk-negative and lyn-negative cells, which is consistent with the loss of calcium release. Taken together, these observations suggest that the defect of p72syk or p53/56lyn was responsible for the abnormality of calcium mobilization in both lyn-negative and syk-negative cells, and that both p72syk and p53/56lyn might regulate calcium mobilization through the phosphatidylinositol pathway in B cell oxidant stress signaling.

Animals↗

Cloning of the human eosinophil chemoattractant, eotaxin. Expression, receptor binding, and functional properties suggest a mechanism for the selective recruitment of eosinophils.

The CC chemokine eotaxin, identified in guinea pigs and also recently in mice, may be a key element for the selective recruitment of eosinophils to certain inflamed tissues. Using a partial mouse eotaxin CDNA probe, the human eotaxin gene was cloned and found to be 61.8 and 63.2% identical at the amino acid level to guinea pig and mouse eotaxin. Human eotaxin protein was a strong and specific eosinophil chemoattractant in vitro and was an effective eosinophil chemoattractant when injected into the skin of a rhesus monkey. Radiolabeled eotaxin was used to identify a high affinity receptor on eosinophils (0.52 nM Kd), expressed at 4.8 x 10(4) sites per cell. This receptor also bound RANTES and monocyte chemotactic protein-3 with lower affinity, but not macrophage inflammatory protein-1 alpha. Eotaxin could desensitize calcium responses of eosinophils to RANTES and monocyte chemotactic protein-3, although RANTES was able to only partially desensitize eosinophil calcium responses to eotaxin. Immunohistochemistry on human nasal polyp with antieotaxin mAbs showed that certain leukocytes as well as respiratory epithelium were intensely immunoreactive, and eosinophil infiltration occurred at sites of eotaxin upregulation. Thus eotaxin in humans is a potent and selective eosinophil chemoattractant that is expressed by a variety cell types in certain inflammatory conditions.

Amino Acid Sequence↗