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At least 415 records · Page 23Linked to original sources
PubMed1989

Allergen-specific induction of interleukin-2 (IL-2) responsiveness in lymphocytes from children with asthma. I. Antigen specificity and initial events of the induction.

Interleukin-2 (IL-2) responsiveness of Dermatophagoides farinae (Df)-stimulated lymphocytes from children with bronchial asthma was studied. Six-day culture of lymphocytes from allergic patients increased after an additional 3 days of incubation with recombinant IL-2. This phenomenon was not observed when the lymphocytes of patients allergic to Df were stimulated with ovalbumin (OVA). Normal lymphocytes stimulated with Df expressed Tac antigen (low-affinity IL-2 receptor) but, in contrast to the patients' lymphocytes, did not absorb nor respond to IL-2. Nonadherent responder cells cultured with Df-pulsed autologous adherent cells acquired IL-2 responsiveness, but those cultured with OVA-pulsed adherent cells did not. The monoclonal antibody to HLA-DQ framework (Leu 10 and clonab DQ), but not to HLA-DR framework (OKIa1) and HLA-DP (HLA-DP and clonab DP-DR), blocked the antigen-presenting cells from inducing IL-2 responsiveness. Nonadherent responder cells depleted of OKT4 (CD4)-positive cells failed to acquire IL-2 responsiveness, whereas depletion of OKT8 (CD8) cells had no impact. Taken as a whole, the results indicate that DQ-bearing adherent cells from allergic donors play a key role in presenting Df antigen to allergen-specific responder T cells, which are very likely to be members of the OKT4 positive subset.

Absorption↗
PubMed2006

PLAC1 mRNA levels in maternal blood at induction of labor correlate negatively with induction-delivery interval.

OBJECTIVE: This study was conducted to determine whether, in low risk women having labor induced using prostaglandin gel (dinoprostone gel), there is a relationship between the concentration of mRNA for the PLAC1 gene (a trophoblast-specific gene) in maternal blood and the time elapsed between the first gel administration and spontaneous delivery. STUDY DESIGN: Blood was collected from 49 selected women at 40.2-41.4 weeks' gestation. Total RNA was extracted by means of an ABI Prism 6100 nucleic acid Prep Station and quantitative real-time PCR analysis was performed by use of a PE Applied Biosystems 5700 Sequence Detection System. Sequence data were obtained from the Genebank Sequence Database. To determine the amount of cDNA, the PLAC1 locus was used. RESULTS: Thirty women (61.2%) had a spontaneous delivery. A caesarean section, either for fetal dystocia or fetal distress, was performed in 19 (38.8%). The crude delivery rates of the women who ended up with a spontaneous delivery were 30% at 24 h and 43% at 48 h. Women (n=19) with a blood concentration of logPLAC1 mRNA>or=2.00 displayed a median time to delivery of 23.50h, (95% CI: 13.13-33.87) while those with a logPLAC1 mRNA<2.00 (n=30) had a median time of 54 h. (95% CI: 37.86-70.14; p=0.0043, log-rank test). By means of multivariate analysis, quantitative Bishop score (from 2 to 7) at the time of the first gel administration and logPLAC1 mRNA>or=2.00 were associated with a higher rate of delivery per unit of time with an odds ratio of 1.35 (95% CI: 1.07-1.71) and 3.48 (95% CI: 1.55-7.80), respectively. CONCLUSIONS: In induced term pregnancies, PLAC1 mRNA in maternal blood at the beginning of the treatment correlates with the time elapsed before delivery. This evidence demonstrates that the fetomaternal trafficking of nucleic acids is more consistent when the labor is about to begin.

Adult↗
PubMed1998

Induction of apoptosis in glioblastoma cells by inhibition of protein kinase C and its association with the rapid accumulation of p53 and induction of the insulin-like growth factor-1-binding protein-3.

Increased protein kinase C(alpha) (PKC(alpha)) expression in glioblastoma cells is associated with proliferation and resistance to drug-induced apoptosis by an undefined anti-apoptotic pathway. To clarify the role of PKC in apoptosis, we have investigated the effect of the selective PKC inhibitor Ro 31-8220 (3-[1-[3-(amidinothio)propyl]-3-indolyl]-4-(1-methyl-3-indolyl)-1H -pyrrole-2,5-dione methanesulfonate) in two glioblastoma cell lines whose proliferation is dependent on high levels of PKC(alpha). U-87 and A172 cells treated with an IC50 of Ro 31-8220 exhibited nucleosomal DNA fragmentation that coincided with an increase in the number of apoptotic cells. This effect was preceded by the rapid nuclear accumulation of wild-type p53 within 2 hr, and an increased level of the pro-apoptotic protein, insulin-like growth factor-1-binding protein-3, (IGFBP3) but not other p53-regulated proteins such as p21WAF1 or Bax. Accumulation of p53 was also associated with the hypophosphorylated and activated form of the retinoblastoma tumor suppressor protein (RB) at later times after treatment. These results suggest that PKC(alpha) suppresses apoptosis in glioblastoma cells primarily by restricting the accumulation of p53 and the expression of insulin-like growth factor-1-binding protein, as well as by maintaining RB in an inactive hyperphosphorylated state.

Apoptosis↗
PubMed2002

Strong induction of tyrosine phosphorylation, intracellular calcium, nuclear transcription factors and interferongamma, but weak induction of IL-2 in naïve T cells stimulated by bacterial superantigen.

The outcome of T cell receptor (TCR) engagement is controlled by the differential recruitment of a variety of pathways, depending on the nature of the TCR ligand. Studies on superantigens (SAGs) were among the first describing such differential signaling; however, reported results are inconsistent. We took a quantitative approach to reinvestigate this question. Using nai;ve T cells from TCR transgenic mice, we found that compared to the antigenic peptide from pigeon cytochrome c, the SAG staphylococcal enterotoxin A very efficiently (100-2000-fold more sensitive on a weight basis) induced tyrosine kinase activity, intracellular calcium increase, and interferon (IFN)gamma production. Up-regulation of CD25 and CD69 and proliferation were less efficiently induced (20-30-fold more sensitive), and interleukin (IL)-2 production was induced least efficiently (only 2-fold more sensitive). This differential activation profile that varies with the activation event analyzed is discussed with respect to the propensity for SAG to induce anergy.

Animals↗
PubMed1983

Induction of suppressor T cells to dinitrofluorobenzene contact sensitivity by application of sensitizer through Langerhans cell-deficient skin. II. Kinetics of the induction of suppressor T cells.

Tolerance to dinitrofluorobenzene (DNFB) contact sensitivity (DNFB CS) appeared in C3H/HeN mice within 2 days after application of DNFB on Langerhans cell-deficient tail skin. A single painting on tail skin led to complete prevention of DNFB CS for at least 14 days. Spleen cells from tolerant mice could transfer the suppression to syngeneic recipients, while the cells treated in vitro with anti-Thy 1.2 lost their suppressive activities completely. From these facts, this tolerance might be due to active suppression caused by suppressor T cells. These suppressor T cells were antigen-specific, because recipients exhibited normal CS to picryl chloride. Furthermore, the suppressor T cells were demonstrated to be afferent blockers in nature and their precursors were sensitive to cyclophosphamide. Therefore, the suppressor T cells induced by DNFB percutaneously administered through epidermal Langerhans cell-deficient region were thought to be generated in the same or in a very similar suppressor pathway as the intravenously administered dinitrobenzene sulfonate (DNBSO3), a soluble reactive dinitrophenyl congener.

Animals↗
PubMed1998

Induction of apoptosis by gemcitabine in BG-1 human ovarian cancer cells compared with induction by staurosporine, paclitaxel and cisplatin.

A variety of chemotherapeutic agents induce cell death via apoptosis. We had shown previously that gemcitabine (2',2'-difluorodeoxycytidine) induced an atypical apoptosis in BG-1 human ovarian cancer cells; therefore, further studies were conducted to characterize more precisely gemcitabine-induced apoptosis in BG-1 cells compared to a general inducer of apoptosis, staurosporine. BG-1 cells exposed to 0.5, 1.0 and 10 microM gemcitabine for 8 h, or staurosporine (1.0 microM) for 6 h, exhibited high molecular weight DNA fragmentation (50 kbp); however, only staurosporine treatment produced internucleosomal DNA fragments (200 bp) in a laddered pattern on the agarose gel. Staurosporine (1.0 microM) rapidly induced phosphatidylserine plasma membrane translocation that increased linearly with time as measured by annexin V-FITC binding, and similar kinetics were observed for caspase activation by staurosporine in BG-1 cells. In contrast, 10 microM gemcitabine increased phosphatidylserine expression in a small fraction of cells (5-10%) vs. untreated controls over the course of 48 h and significant caspase activity was detected within 12 h of drug exposure. Time-lapse video microscopy of BG-1 cells exposed to 1.0 microM staurosporine or 10 microM gemcitabine for up to 72 h showed that the morphologic changes and kinetics of cell death induced by these agents differed significantly. We also evaluated the apoptosis induced by paclitaxel (a mitotic poison) and cisplatin (an agent not dependent on cell cycle functions) in BG-1 cells by these methods because these drugs are used clinically to treat ovarian cancer. Our findings demonstrate that the kinetics of apoptotic cell death induced by gemcitabine and other chemotherapeutic agents should be taken into account when designing treatment strategies for ovarian cancer.

Journal Article↗
PubMed1998

Gadolinium determination in tissue samples by inductively coupled plasma mass spectrometry and inductively coupled plasma atomic emission spectrometry in evaluation of the action of magnetic resonance imaging contrast agents.

The quantitative determination of Gd-containing magnetic resonance imaging (MRI) contrast agents in animal tissues is performed by both ICP-AES and ICP-MS. While ICP-AES has been used to determine Gd-containing contrast agents by other workers, no published methodology has been found. An accurate and precise method using nitric acid and microwave digestion for sample preparation is described. Dosed rat tissue, blood and plasma were measured by both ICP-AES and ICP-MS. The ICP-AES method is excellent for screening Gd levels and quantitative determination of concentrations above 400 ng ml-1, but it lacks the sensitivity to measure agent concentrations in low dose MRI studies. This work demonstrates that ICP-MS has the needed sensitivity to replace radiotracer methods currently used for low dose studies, while maintaining the accuracy and precision of results obtained by ICP-AES. Gadolinium detection limits in tissue were 0.04 mumol of Gd per kg of tissue, an order of magnitude lower than studies using radiotracer techniques.

Animals↗