Biomedical subjects

Q Ge

Publications and source records attributed to Q Ge.

At least 19 recordsLinked to original sources

PubMed2005

Inflammatory mediator release in normal bronchial smooth muscle cells is altered by pregnant maternal and fetal plasma independent of asthma.

Studies have shown that pregnancy can alter the pathophysiology of a pre-existing maternal disease such as asthma. However, the mechanisms that alter maternal asthma during pregnancy are presently unknown. Previous work has demonstrated that human bronchial smooth muscle (BSM) cells produce inflammatory factors in response to nonpregnant, atopic plasma. The aim of this study was to determine whether circulating pregnancy-derived factors in maternal and fetal plasma can stimulate inflammatory mediator release in BSM cells in the presence and absence of maternal asthma. Cultured human BSM cells were exposed to maternal and fetal plasma from normal pregnancies and pregnancies complicated by asthma. Inflammatory mediator release was determined by enzyme-linked immunosorbent assay (ELISA). Both maternal and fetal plasma from asthmatic and nonasthmatic individuals significantly increased production of interleukin (IL)-6 (ANOVA, P<0.001), regulated upon activation, normal T-cell expressed and secreted (RANTES) (ANOVA, P<0.01), and soluble intercellular cell-adhesion molecule-1 (sICAM-1) (ANOVA, P<0.01). There was no difference in inflammatory mediator release in response to asthma and nonasthmatic plasma. Eotaxin release was increased by pregnant asthmatic plasma (ANOVA, P<0.05). The results of this study suggest that circulating pregnancy-related factors can activate asthma-associated mediators in BSM cells. This change in BSM function may be one mechanism that contributes to increased asthma severity during pregnancy.

Asthma↗

PubMed2005

In vitro studies of lymphangioleiomyomatosis.

Lymphangioleiomyomatosis (LAM) is associated with abnormal airway smooth muscle that leads to the characteristic pathology of lung nodule formation and destruction of lung tissue. The current authors have previously identified abnormal behaviour of airway smooth muscle cells from patients with asthma. In this study, cells and tissue sections derived from patients with LAM (n=7), asthma (n=8), and nonasthmatic controls (n=9) were compared. The presence of the antigen human melanosome (HM)B-45 was investigated, along with the proliferation and release of extracellular matrix proteins, release of endogenous prostaglandin E2 (PGE2), vascular endothelial growth factor and connective tissue growth factor, and the expression of integrins. Positive HMB-45 staining was found in all LAM patients and no controls. Proliferation of LAM cells was not different from control cells nor was its inhibition by beta-agonists, corticosteroids, rapamycin or PGE2. However, endogenous PGE2 levels were markedly decreased in LAM cells, and this was associated with decreased expression of the inducible form of cyclooxygenase (COX-2). The increased levels of connective tissue growth factor seen in asthma cells were not observed in LAM. Elastin mRNA in response to transforming growth factor-beta stimulation was markedly lower in LAM cells than either asthma or control cells. In conclusion, lymphangioleiomyomatosis cells exhibit abnormal properties in vitro that may contribute to pathophysiology and symptomatology in patients with lymphangioleiomyomatosis.

Adolescent↗

PubMed2004

Structure dependence of NO adsorption and dissociation on platinum surfaces.

The influence of surface structure on NO chemisorption and dissociation on Pt[100]-(1x1), Pt[211], and Pt[410] has been studied using density functional theory slab calculations with the generalized gradient corrections. The presence of steps on Pt[211] strengthens the NO-surface chemisorption bond, but the barrier for NO dissociation remains high. On the other hand, the steps on Pt[410] help to stabilize the N and O adatoms that form upon dissociation and the transition state. The calculated barrier of 80.2 kJ/mol on Pt[410] is in good agreement with experiment. These results show that both the presence of steps and the nature of the steps are important to activate NO. An ensemble of square-arranged Pt atoms has been identified as an important feature in activating the N-O bond.

Journal Article↗

PubMed2004

Mechanisms of serum potentiation of GM-CSF production by human airway smooth muscle cells.

Inflammation and vascular leakage are prevalent in asthma. This study aimed to elucidate the mechanisms involved in serum potentiation of cytokine-induced granulocyte macrophage colony stimulating factor (GM-CSF) production by human airway smooth muscle cells and to identify possible factors responsible. Serum-deprived cells at low density were stimulated with TNF-alpha and IL-1beta for 24 h. Human AB serum (10%), inhibitors of RNA and protein synthesis or specific signaling molecules, or known smooth muscle mitogens were then added for 24 h. Culture supernatants were analyzed for GM-CSF levels, and cells were harvested to assess viability, cell cycle progression, GM-CSF-specific mRNA content, and p38 phosphorylation. Serum potentiated GM-CSF release when added before, together with (maximal), or after the cytokines. The potentiation involved both new GM-CSF-specific mRNA production and protein synthesis. The mitogens IGF, PDGF, and thrombin all potentiated GM-CSF release, and neutralizing antibodies for EGF, IGF, and PDGF reduced the serum potentiation. Inhibitor studies ruled as unlikely the involvement of p70(S6kinase) and the MAPK p42/p44, two signaling pathways implicated in proliferation, and the involvement of the MAPK JNK, while establishing roles for p38 MAPK and NF-kappaB in the potentiation of GM-CSF release. Detection of significant p38 phosphorylation in response to serum stimulation, through Western blotting, further demonstrated the involvement of p38. These studies have provided evidence to support p38 being targeted to interrupt the cycle of inflammation, vascular leakage and cytokine production in asthma.

Antibodies↗

PubMed2001

Partial and generalized epilepsy with febrile seizures plus and a novel SCN1A mutation.

BACKGROUND: Generalized epilepsy with febrile seizures plus (GEFS+) is an autosomal dominant syndrome characterized by febrile seizures (FS) and a variety of afebrile generalized seizure types. GEFS+ has previously been linked to mutations in two genes encoding the voltage-gated sodium channel alpha-subunit (SCN1A) and beta1-subunit (SCN1B). We studied a large family with FS and partial as well as generalized seizure types. METHODS: All but two living affected family members were interviewed and examined. Information on deceased affected family members was sought. EEG for 11 affected family members and one unaffected family member were obtained. Genetic linkage analysis and mutation screening of SCN1A were performed on blood samples from 16 affected individuals and their first-degree relatives. RESULTS: There were 27 affected family members; 18 were alive at the time of the study. All affected family members had FS; seven had FS only, and 19 also had afebrile seizures. Eleven individuals continued to have FS beyond 6 years of age. FS were complex in 12 family members, usually with prolonged duration. The index patient had right temporal lobe epilepsy and hippocampal sclerosis. Four other patients had strong historical evidence of temporal lobe epilepsy, and three others had nonlocalizing evidence of partial epilepsy. Pedigree analysis indicated autosomal dominant transmission. All affected individuals who were tested and one asymptomatic individual had a sodium channel mutation of SCN1A, an A-->C transversion at nucleotide 3809 resulting in the substitution of lysine 1270 by threonine in the D3/S2 segment (designated as K1270T). CONCLUSIONS: Our findings indicate that partial epilepsy preceded by FS can be associated with sodium channel mutations and may represent a variant of GEFS+.

Adolescent↗

PubMed2001

Airway smooth muscle cell proliferation is increased in asthma.

UNLABELLED: Increased airway smooth muscle (ASM) within the bronchial wall of asthmatic patients has been well documented and is likely to be the result of increased muscle proliferation. We have for the first time been able to culture ASM cells from asthmatic patients and to compare their proliferation rate with that of nonasthmatic patients. Asthmatic ASM cell cultures (n = 12) were established from explanted lungs and endobronchial biopsies. Nonasthmatic ASM cells (n = 10) were obtained from explanted tissue from patients with no airway disease, emphysema, carcinoma, and fibrosing alveolitis. Cell counts, tritiated thymidine incorporation, and cell cycle analysis were conducted over 7 d. Asthmatic ASM cell numbers at Days 3, 5, and 7 were significantly higher than corresponding values for nonasthmatic cells (p < 0.05). Tritiated thymidine incorporation was increased 3.2-fold in asthmatic cells compared with nonasthmatic cells within the first 24 h (p = 0.026). Flow cytometric analysis of DNA content on Days 1 and 2 revealed that a significantly greater percentage of asthmatic ASM cells were in the G2 + M phase (p < 0.05). This study shows for the first time that proliferation of ASM cells is increased in patients with asthma and provides evidence for an intrinsic abnormality in the ASM cell in this disease. KEYWORDS: asthma; human airway smooth muscle; cell culture; cell proliferation; hyperplasia

Adolescent↗

PubMed2001

Dislocation-controlled perforated layer phase in a PEO- b-PS diblock copolymer.

Small angle x-ray analyses show that the shear-induced hexagonal perforated layer phase in a poly(ethylene oxide)- b-polystyrene diblock copolymer consists of trigonal (R3;m) twins and a hexagonal (P6(3)/mmc) structure, with trigonal twins being majority components. Transmission electron microscopy reveals that the hexagonal structure is generated through sequential intrinsic stacking faults on the second layer from a previous edge dislocation line, while the trigonal twins are formed by successive intrinsic stacking faults on neighboring layers due to the plastic deformation under mechanical shear.

Journal Article↗

PubMed2001

Dependence of lymphopenia-induced T cell proliferation on the abundance of peptide/ MHC epitopes and strength of their interaction with T cell receptors.

Factors that affect naive T cell proliferation in syngeneic lymphopenic hosts were investigated. 2C T cell receptor (TCR) transgenic T cells lacking both CD8 and CD4 survived but hardly proliferated. Proliferation of CD8(+) 2C cells was proportional to the abundance of cognate peptide/MHC complexes and was severely inhibited by injection of anti-CD8 antibody. Weakly reactive self-peptides slightly enhanced CD8(+) 2C cell proliferation whereas a potent agonist peptide promoted much more rapid proliferation, but inflammation-stimulating adjuvant had only a small effect on the rate of cell proliferation. The findings suggest that under uniform lymphopenic conditions, the widely different rates of proliferation of T cells expressing various TCR, or the same TCR in the presence or absence of CD8, reflect the strength of interaction between TCR and MHC associated with particular self-peptides.

Animals↗

PubMed2001

The role of sexual related Y gene detection in the diagnosis of patients with gonadal dysgenesis.

OBJECTIVE: To clarify the role of sexual related Y (SRY) gene detection in the diagnosis of gonadal dysgenesis. METHODS: Sixteen cases of gonadal dysgenesis were included in this study: 5 with androgen insensitivity syndrome, 1 with 17-alpha-hydroxylase deficiency, 4 with true hermaphrodite, 2 with 45, X/46, XY gonadal dysgenesis, 1 with 45, X gonadal dysgenesis, 1 with XY pure gonadal dysgenesis, 1 with testicular regression, and 1 XY female who gave birth to a normal baby. SRY gene was detected by using polymerase chain reaction (PCR) in blood and gonad samples and by direct sequencing of the SRY motif. RESULTS: Among the 16 cases, 15 were blood SRY positive, among which 13 (86.7%) showed the presence of testicular tissue, and 2 showed ovaries without testicular tissue. One SRY negative case showed the presence of testicular tissue. In 3 cases, SRY detection in gonadal tissue correlated with pathological findings but not with blood karyotype. The correlation between peripheral blood SRY and the pathology of the gonads was 81.25% and the correlation between the presence of peripheral blood Y chromosome and pathology of the gonads was 68.75%. Sequencing of the SRY motif in an XY female who gave birth to a normal baby showed no mutation. CONCLUSIONS: SRY detection is more sensitive and specific than blood karyotype in the prediction of the presence of testicular tissue. Peripheral blood karyotype does not necessarily reflect gonadal type. There may be testicular related factors other than the SRY gene.

DNA↗

PubMed2000

Homeostasis-stimulated proliferation drives naive T cells to differentiate directly into memory T cells.

The developmental requirements for immunological memory, a central feature of adaptive immune responses, is largely obscure. We show that as naive CD8 T cells undergo homeostasis-driven proliferation in lymphopenic mice in the absence of overt antigenic stimulation, they progressively acquire phenotypic and functional characteristics of antigen-induced memory CD8 T cells. Thus, the homeostasis-induced memory CD8 T cells express typical memory cell markers, lyse target cells directly in vitro and in vivo, respond to lower doses of antigen than naive cells, and secrete interferon gamma faster upon restimulation. Like antigen-induced memory T cell differentiation, the homeostasis-driven process requires T cell proliferation and, initially, the presence of appropriate restricting major histocompatibility complexes, but it differs by occurring without effector cell formation and without requiring interleukin 2 or costimulation via CD28. These findings define repetitive cell division plus T cell receptor ligation as the basic requirements for naive to memory T cell differentiation.

Adoptive Transfer↗

PubMed2000

Apoptotic cells actively inhibit the expression of CD69 on Con A activated T lymphocytes.

Although apoptosis is commonly viewed as a silent cell death without damage to adjacent tissues, the effect of apoptosis on immunity has been unclear. We have investigated the influence of apoptotic cells on T-cell activation. The K562 or HL-60 human leukemia cell lines that had been induced apoptosis by FTY720 or cycloheximide (CHX) were added into the culture of mouse spleen cells stimulated with Con A. Six to 20 h later, the expression of CD69, an early T-cell activation antigen, was detected using flowcytometry. Living cells and necrotic cells served as control groups. Apoptotic K562 or HL-60 cells induced by either FTY720 or CHX unanimously inhibited CD69 expression on the CD3+ mouse T cells while living and necrotic cells did not. The inhibition was proportional to the number of apoptotic cells and was different in the T-cell subsets, showing a rapid and transient inhibition on the CD3+CD8+ T-cell activation but with a slow and continuous inhibition on CD3+CD8- T-cell activation. In conclusion, the apoptotic cells actively inhibit a T-cell activation that is independent of the cell lines or the apoptotic inducers, indicating that the apoptotic cells dominantly regulate T-cell immunity.

Animals↗

PubMed2000

Effect of murine thymic epithelial cell line (MTEC1) on the functional expression of CD4(+)CD8(-) thymocyte subgroups.

To determine the effect of thymic stromal cells on the functional maturation of CD4 single-positive (SP) thymocytes, the functional status of isolated CD4 SP thymocyte subgroups was investigated by means of cell proliferation and cytokine production in response to concanavalin A (Con A) prior and after co-culturing with a murine thymic epithelial cell line (MTEC1). Mouse medullary CD4 SP thymocytes were phenotypically divided into seven discrete subgroups predicted to reflect the maturation pathway from newly emerging CD4 SP thymocytes to terminally differentiated cells. For functional analysis, six major subgroups (6C10(+)CD69(+), 6C10(-)CD69(+), 6C10(-)CD69(-)3G11(+)Qa-2(-), 6C10(-)CD69(-)3G11(+)Qa-2(+), 6C10(-)CD69(-)3G11(-)Qa-2(-) and 6C10(-)CD69(-)3G11(-)Qa-2(+)) cells were isolated and their functional status in response to Con A stimulation assessed. A functional hierarchy is revealed among these subgroups, consistent with their phenotypic maturation status, which may imply that these cells undergo a functional maturation process within thymic medulla. The function of cytokine production by CD4 SP thymocytes is acquired in a stepwise manner from a low to high level and characterized by T(h)0-type cytokines in the main stream of differentiation pathway. However, a minor subgroup that appeared at the late stage as 3G11(-)6C10(-) cells was biased to produce T(h)2-type cytokines. Nevertheless, the functional capacity of the final two Qa-2(+) subgroups of CD4 SP thymocytes was still significantly lower than that of spleen CD4(+) T cells. After co-cultivation with MTEC1 cells, four subgroups of TCRalphabeta(+)CD4(+)CD8(-) thymocytes exhibited significantly higher levels of proliferation capability and modulation in cytokine production capability. However, co-culturing with MTEC1 cells did not change the pattern of T(h)0- or T(h)2-like cytokine production by respectively medullary CD4 SP thymocyte subgroups nor could MTEC1 induce CD4 SP thymocytes to secrete T(h)1-type cytokines. The results suggest that MTEC1 can regulate the functional status of these thymocyte subgroups.

Animals↗

PubMed2000

The production of extracellular matrix proteins by human passively sensitized airway smooth-muscle cells in culture: the effect of beclomethasone.

Airway remodeling is a key feature of persistent asthma. Part of the remodeling process involves the laying down of extracellular matrix (ECM) proteins within the airways. In this study we compared the production of ECM proteins by human airway smooth-muscle (ASM) cells in culture after exposure to 10% serum from an asthmatic individual or 10% serum from a nonasthmatic individual with or without beclomethasone (0.01 to 100 nM). Enzyme-linked immunosorbent assays were done with antibodies to human fibronectin; perlecan; elastin; the laminin beta(1), gamma(1), beta(2), alpha(1) chains; thrombospondin; chondroitin sulfate; collagen types I, III, IV, and V; versican; and decorin. Serum from the asthmatic individual, when compared with that from the nonasthmatic individual, caused a significant increase in the production of fibronectin, perlecan, laminin gamma(1), and chondroitin sulfate. Beclomethasone caused a significant reduction in the number of cells exposed to serum from either the asthmatic or nonasthmatic individual, but did not reverse the increase in ECM protein induced by the former. These results suggest an interaction between the ASM and the allergic process that may alter components of the airway wall in asthma, and that corticosteroids may not prevent the fibrosis induced by resident cells within the airways.

Adult↗

PubMed2000

[Application of mitotic index and proliferating cell nuclear antigen index in monitoring the change of rat endometrium after administration of estrogen and progestin].

OBJECTIVE: To investigate the mitotic index (MI) and proliferating cell nuclear antigen (PCNA) index in monitoring the rat endometrium during estrogen and progestin administration. METHODS: One hundred and sixty Sprague-Dolly rats were randomly divided into seven groups. The 1st and 2nd group were normal estrous (E) and ovariectomized (OVX) control. The other groups received estradiol (E2V) only or combined with medroxyprogesterone(MPA) which imitated the clinical regimen in different dosage and different time before sacrificed. Uteri sections were stained with HE and immunohistochemical procedures to detect mitosis and PCNA. RESULTS: The MI and PCNA index were similar in the luminal and glandular cells. Both markers were low in the two control groups and increased with the E2V dosage in the treatment group. But if E2V was given for 1 to 21 days, the MI increased during the first 3 days and then dropped to low level and kept to the end. PCNA index increased in the first 3 days and decreased to a low level on the 4th day and then increased gradually to a high level until the last day. In the continuous regimen, both markers decreased as the MPA dosage increased. In the cyclic regimen, The MI reached to a significant low level nearly to zero in almost each ratio. Addition of MPA for 10 days, PCNA index at the ratio of 1:4.0 could be reduced to a low level and addition for 5 days, PCNA index in each subgroup was still as high as the positive control even though the dosage of MPA increased several times to 1:8.0. CONCLUSIONS: This study suggests that PCNA index can reflect both the effect of estrogen and progestogen. PCNA index is better than mitotic index in reflecting the change of endometrium.

Animals↗

PubMed1999

Phenotypic identification of the subgroups of murine T-cell receptor alphabeta+ CD4+ CD8- thymocytes and its implication in the late stage of thymocyte development.

Phenotypic analysis of the medullary-type CD4+ CD8- [CD4 single-positive (SP)] thymocytes has revealed phenotypic heterogeneity within this cell population. The characteristic phenotype of mature peripheral T cells can be uniquely marked as Qa-2+ HSA- CD69-, whereas in the medullary-type CD4 SP thymocytes, the expression patterns of many markers were quite different. This suggests that there are many subgroups in the population, which reflects that medullary-type CD4 SP thymocytes may undergo phenotypic maturation. According to the results of two-colour flow cytometry, seven discrete phenotypes were identified by the expression capacity of Qa-2, HSA, CD69, 3G11 and 6C10 molecules. Consequently, the phenotypic precursor-progeny relationship can be envisaged as: 3G11- 6C10+ CD69+ HSAhi -->3G11+ 6C10+ CD69+ HSAhi --> 3G11+ 6C10- CD69+ HSAint -->3G11+ 6C10- CD69- HSAint Qa-2- -->3G11+ HSA-/lo Qa-2lo. At the stage of 3G11+ 6C10- CD69- HSAint Qa-2-, a branch pathway could be initiated, which gave rise to 3G11- HSAl degrees Qa-2- cells, which then, in turn, developed into 3G11- HSA-/loQa-2hi cells, a minor subgroup of the most mature CD4 SP cells. Consistent with this predicted pathway, experiments indicated that the first two subgroups were still cortisone sensitive, whereas the others were cortisone resistant. The cells in the last two Qa-2-positive subgroups are probably ready for emigration into the periphery.

Animals↗

PubMed1999

Spontaneous activation of hamster oocytes in vitro.

OBJECTIVES: To observe the time of spontaneous activation of hamster oocytes and to find out the early signs of hamster oocytes activation. METHODS: First, 63 hamster oocytes including activated and non-activated oocytes (group A) and 51 non-activated oocytes (group B) were injected with human sperm and checked for fertilization after 16-18 hours. Then, 20 hamster oocytes were cultured in vitro in medium with or without calcium and examined under light microscope every half an hour up to 9 hours. RESULTS: Under light microscope, hamster oocytes activation were observed to undergo 4 stages: metaphase II stage without meiotic spindle, appearance of meiotic spindle near the first polar body, protrusion of oolemma, and complete extrusion of second polar body with pronucleus formation. After culture for 1.5 hours in vitro, 30%-40% of the oocytes demonstrated meiotic spindle; but after 9 hours, 50% showed complete activation. Culture in medium without calcium showed a little delay in the process of activation. The earliest sign of spontaneous activation in hamster oocytes was the appearance of meiotic spindle near the first polar body. Although group A and B showed no difference, the damage rate was lower in group B (19.7% +/- 16.6%) than in group A (35.9% +/- 5.7%) (P = 0.08), whereas the fertilization rate (18.3% +/- 10.9%) was higher in group B than in group A (14.2% +/- 8.7%) (P = 0.135). CONCLUSIONS: Hamster oocytes may be activated spontaneously early after their removal. It is important to recognize the earliest sign of spontaneous activation and perform intracytoplasmic sperm injection (ICSI) before it happens.

Animals↗

PubMed1999

[Phenotypic analysis of TCR alpha beta+ CD4+CD8- medullary thymocytes].

Phenotypic analysis of the medullary-type CD4+CD8- (CD4SP) thymocytes have revealed phenotypic heterogeneity within these cells. The phenotype of mature peripheral T cells is Qa-2+ HSA- CD69-, whereas in the medullary-type CD4SP thymocytes, the expression pattern of many markers were quite different, suggesting that the medullary-type CD4SP thymocytes may undergo phenotypic maturation. According to the results of two-color cytometry, seven discrete phenotypes were defined by the relative expression of Qa-2, HSA, CD69, 3G11 and 6C10: 3G11-6C10+CD69+HSAhi-->3G11+6C10+CD69+ HSAhi-->3G11+6C10-CD69+HSAint-->3G11+6C10- CD69-HSAint Qa-2(-)-->3G11+HSAlo/-Qa-2lo, at the same time, 3G11+6C10-CD69-HSAint Qa-2(-)-->3G11-HSAlo Qa-2(-)-->3G11-HSAlo/- Qa-2hi, the last two Qa-2 positive subsets could exit the thymus and home into periphery.

Animals↗

PubMed1999

[The effects of sex hormone on blood vessels].

OBJECTIVE: The protective mechanism of sex hormone on blood vessels was investigated to provide evidences for clinical use of hormone replacement therapy in postmenopausal women. METHODS: To observe the effects of 17 beta-estradiol (E2), progesterone(P), testosterone (T) and E2 combined with P on the relaxation of umbilical arterial rings (UAR) as well as production of nitric oxide (NO) in cultured umbilical endothelial cells(HUVEC) in vitro. RESULTS: The results showed that 10(-9)-10(-6) mol/L E2 dilation of UAR, but 10(-5) mol/L E2 showed vague effect. P or T had no relaxation effect, but releasing nitric oxide. When in combined trial P at 10(-5) mol/L inhibited the relaxation effect of E2 at 10(-7)-10(-5) mol/L but didn't inhibit E2 10(-9) mol/L. In HUVEC 10(-9)-10(-5) mol/L E2 stimulated the release of nitric oxide when cells incubated for 10 min and 30 min, but did not influence the NO release at 60 min. P and T have different effects on the release of nitric oxide at different concentrations and incubation time. P also inhibited the NO release induced by E2. CONCLUSIONS: The results indicated that P actually inhibited the relaxation response and induction of NO release by E2, especially at the high concentration. Therefore, we suggested that to use low doses of E2 combined with low dose P for hormone replacement therapy in prevention and treatment of cardiovascular diseases in postmenopausal patient.

Cells, Cultured↗