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PubMed2003

Possible overestimation of indocyanine green-derived plasma volume early after induction of anesthesia with propofol/fentanyl.

UNLABELLED: Apparently large plasma volumes derived by indocyanine green (PV-ICG) have been determined in the initial period after induction of anesthesia. We tested the hypothesis that possible overestimation of PV-ICG occurs shortly after anesthetic induction. Anesthesia was induced in 13 patients with fentanyl bolus 2 microg/kg and propofol infusion 0.5 mg x kg(-1) x min(-1) IV until patients lost consciousness and was then maintained with a propofol infusion. PV-ICG and the initial distribution volume of glucose (IDVG) were assessed at 15 min before and at 15 min after anesthetic induction. Plasma ICG and glucose concentrations were measured from serial blood samples taken before and through 7 min after injection of ICG 25 mg and glucose 5 g. PV-ICG and IDVG were calculated using a one-compartment model. PV-ICG was significantly increased by an average of 15.3% after induction, from 2.29 +/- 0.38 (SD) L to 2.64 +/- 0.31 L (P < 0.001). The mean hematocrit (Hct), concentrations of hemoglobin (Hb), and total plasma proteins at postinduction decreased compared with those at preinduction by 2.9%, 2.2%, and 2.3%, respectively (P < 0.05). Percentile increase in plasma volume calculated from Hb and Hct before and after induction was 4%. Consequently, an 11% overestimation in PV-ICG was observed. IDVG remained unchanged. Therefore, the ratio of PV-ICG/IDVG increased from 0.40 +/- 0.05 before induction to 0.48 +/- 0.06 after induction (P < 0.01). These results validate the hypothesis that possible overestimation of PV-ICG occurs during a definable period of time after propofol anesthetic induction. The present results also support the PV-ICG/IDVG ratio as a measure of possible overestimation of PV-ICG or fluid redistribution from the central to the peripheral tissues. IMPLICATIONS: An approximate 11% overestimation in indocyanine green derived plasma volume was observed after induction of anesthesia using propofol and fentanyl. Simultaneous measurement of the initial distribution volume of glucose may help investigate the presence of overestimation in indocyanine green derived plasma volume.

Adolescent↗
PubMed2005

Predictors of hypotension after induction of general anesthesia.

Hypotension after induction of general anesthesia is a common event. In the current investigation, we sought to identify the predictors of clinically significant hypotension after the induction of general anesthesia. Computerized anesthesia records of 4096 patients undergoing general anesthesia were queried for arterial blood pressure (BP), demographic information, preoperative drug history, and anesthetic induction regimen. The median BP was determined preinduction and for 0-5 and 5-10 min postinduction of anesthesia. Hypotension was defined as either: mean arterial blood pressure (MAP) decrease of >40% and MAP <70 mm Hg or MAP <60 mm Hg. Overall, 9% of patients experienced severe hypotension 0-10 min postinduction of general anesthesia. Hypotension was more prevalent in the second half of the 0-10 min interval after anesthetic induction (P < 0.001). In 2406 patients with retrievable outcome data, prolonged postoperative stay and/or death was more common in patients with versus those without postinduction hypotension (13.3% and 8.6%, respectively, multivariate P < 0.02). Statistically significant multivariate predictors of hypotension 0-10 min after anesthetic induction included: ASA III-V, baseline MAP <70 mm Hg, age > or =50 yr, the use of propofol for induction of anesthesia, and increasing induction dosage of fentanyl. Smaller doses of propofol, etomidate, and thiopental were not associated with less hypotension. To avoid severe hypotension, alternatives to propofol anesthetic induction (e.g., etomidate) should be considered in patients older than 50 yr of age with ASA physical status > or =3. We conclude that it is advisable to avoid propofol induction in patients who present with baseline MAP <70 mm Hg.

Adult↗
PubMed2003

Neural crest induction by paraxial mesoderm in Xenopus embryos requires FGF signals.

At the border of the neural plate, the induction of the neural crest can be achieved by interactions with the epidermis, or with the underlying mesoderm. Wnt signals are required for the inducing activity of the epidermis in chick and amphibian embryos. Here, we analyze the molecular mechanisms of neural crest induction by the mesoderm in Xenopus embryos. Using a recombination assay, we show that prospective paraxial mesoderm induces a panel of neural crest markers (Slug, FoxD3, Zic5 and Sox9), whereas the future axial mesoderm only induces a subset of these genes. This induction is blocked by a dominant negative (dn) form of FGFR1. However, neither dnFGFR4a nor inhibition of Wnt signaling prevents neural crest induction in this system. Among the FGFs, FGF8 is strongly expressed by the paraxial mesoderm. FGF8 is sufficient to induce the neural crest markers FoxD3, Sox9 and Zic5 transiently in the animal cap assay. In vivo, FGF8 injections also expand the Slug expression domain. This suggests that FGF8 can initiate neural crest formation and cooperates with other DLMZ-derived factors to maintain and complete neural crest induction. In contrast to Wnts, eFGF or bFGF, FGF8 elicits neural crest induction in the absence of mesoderm induction and without a requirement for BMP antagonists. In vivo, it is difficult to dissociate the roles of FGF and WNT factors in mesoderm induction and neural patterning. We show that, in most cases, effects on neural crest formation were parallel to altered mesoderm or neural development. However, neural and neural crest patterning can be dissociated experimentally using different dominant-negative manipulations: while Nfz8 blocks both posterior neural plate formation and neural crest formation, dnFGFR4a blocks neural patterning without blocking neural crest formation. These results suggest that different signal transduction mechanisms may be used in neural crest induction, and anteroposterior neural patterning.

Animals↗
PubMed2000

Induction of heat shock protein 70 by herbimycin A and cyclopentenone prostaglandins in smooth muscle cells.

This study characterizes Hsp70 induction in human smooth muscle cells (SMC) by herbimycin A and cyclopentenone prostaglandins. The magnitude of Hsp70 induction by cyclopentenone prostaglandins was 8- to 10-fold higher than induction by herbimycin A. Hsp70 induction by delta12PGJ2 was first observed at 10 microM, rose to 4000-5000 ng/mL within one log unit and a maximum response was not observed; concentrations of delta12PGJ2 higher than 30 microM were toxic to the cells. A maximum response with herbimycin A (500 ng/mL) was reached at 0.05 microM and maintained to 1 microM without toxicity. Both, delta12PGJ2 and herbimycin A, were inhibited by dithiothreitol (DTT, 100 microM) at lower concentrations and became less sensitive to inhibition at higher concentrations. Hsp70 induction after incubation of SMC with delta12PGJ2 followed by addition of herbimycin A was significantly higher than Hsp70 induction after incubation with herbimycin A followed by addition of delta12PGJ2. When cells were incubated with [3H]-PGJ2, followed by protein denaturation, substantial radioactivity remained protein-bound suggesting that the prostaglandin must be covalently bound. Covalent binding was largely insensitive to DTT. Maximal Hsp70 induction was observed after 5 minutes of exposure of the cells to herbimycin A followed by a 20 hour recovery period in agent-free medium. Cells required 3-4 hours of exposure to delta12PGJ2 followed by a 20 hour recovery period in order to see high Hsp70 induction. Binding of the heat shock factor (HSF) to the heat shock element (HSE) in the presence of herbimycin A or delta12PGJ2, and the effects of DTT, mirrored the results of Hsp70 induction. The results suggest that probable differences between the 2 agents are at the level of the signal transduction prior to HSF activation.

Anti-Bacterial Agents↗
PubMed1979

Comparison of avidin induction in the differentiated and undifferentiated chick oviduct by progesterone, actinomycin D and oviductal injury.

Various oestrogen (diethylstilboestrol, DES) pre-treatments were carried out on chicks and the production of avidin in the oviduct was induced by progesterone, actinomycin D or oviductal injury. Avidin induction was dose-dependent at doses between 5 mg and 40 mg progesterone/kg or 50 micrograns and 300 micrograms actinomycin D/kg respectively. The induction by oviductal injury correlated with the magnitude of tissue injury. First signs of avidin induction were seen at 4 h after oviductal injury, 12 h after progesterone or 12--16h after actinomycin D administration. Actinomycin D (200 micrograms/kg), when administered after progesterone injection, did not increase avidin induction by progesterone, this indicating that avidin induction by actinomycin D is not a "superinduction" effect. Evidence is presented here that the mechanism of avidin induction by oviductal injury and actinomycin D differs from that by progesterone. The differentiation of the oviduct caused by DES treatment was necessary for the induction by progesterone, whereas actinomycin D and oviductal injury also induced avidin in the undifferentiated or poorly differentiated oviduct. Simultaneous DES stimulation potentiated induction by progesterone but not by actinomycin D or oviductal injury. Furthermore, single prior DES stimulation increased avidin induction in the differentiated oviduct of DES-withdrawn chicks caused by progesterone but not that by actinomycin D or oviductal injury.

Animals↗
PubMed1995

Probing collinearity bias in the close induction field.

The substrates of the Poggendorff illusion can be evaluated using as few as two line segments, a test segment whose collinearity is judged, and an induction segment which serves to bias that judgment. Previous research from this laboratory has shown that a very short induction segment can produce a substantial bias of perceived collinearity when it is centered at the tip of the test segment, and there is some evidence that the symmetry of this configuration affects the strength of this bias. Four experiments were conducted to clarify the issue of symmetry in the stimulation of the "half-field" zones which lie on each side of the tip. That Exp. 1a showed displacements which moved the induction segment to an eccentric position, i.e., occupying a single half-field, reduced collinearity error. With additional displacement which produced a gap there was a rebound of induction effect. Exp. 1b indicated that an eccentric induction segment does not produce the usual strength or pattern of bias as a function of its orientation relative to the test segment. Exp. 2a suggested that the strength of induction effect is a function of symmetry within the half-fields rather than the lengths of the segments per se. Finally, in Exp. 2b the strength of induction was a joint function of the position of a short segment within one half-field and the length of another segment which stimulated the other half-field. The effect showed a complex oscillation with changes in position. We discuss the induction mechanism as beginning with "contour filters" which register the induction segment(s) and which combine their responses on the basis of "tandem activation" of the close half-fields.

Form Perception↗
PubMed2003

Focal adhesion kinase is required, but not sufficient, for the induction of long-term potentiation in dentate gyrus neurons in vivo.

Tyrosine kinase phosphorylation plays an important role in the induction of long-term potentiation (LTP). Focal adhesion kinase (FAK) is a 125 kDa nonreceptor tyrosine kinase that shows decreased phosphorylation in fyn mutant mice, and Fyn plays a critical role in LTP induction. By examining the role of FAK involved in LTP induction in dentate gyrus in vivo with medial perforant path stimulation, we found that both FAK and mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) phosphorylation were increased significantly 5 and 10 min after LTP induction, whereas cAMP-responsive element binding protein (CREB) phosphorylation was increased 40 min later. Transfection of the dominant-negative FAK mutant construct HA-FAK(Y397F) impaired LTP, whereas transfection of the constitutively activated form HA-FAK(Delta1-100) reduced the threshold for LTP induction. Transfection of HA-FAK(Delta1-100) by itself did not induce long-lasting potentiation. Further, transfection of the HA-FAK(Y397F) construct decreased FAK, MAPK/ERK, and CREB phosphorylation, and the inhibition of MAPK/ERK decreased CREB phosphorylation. Moreover, blockade of NMDA receptor (NMDAR) did not decrease FAK, MAPK/ERK, and CREB phosphorylation although LTP induction was blunted by NMDAR antagonist. These biochemical changes were not associated with low-frequency stimulation either. Immunoprecipitation results revealed that tyrosine phosphorylation of NR2A and NR2B as well as the association of phosphorylated FAK with NR2A and NR2B was increased with LTP induction. These results together suggest that FAK is required, but not sufficient, for the induction of LTP in a NMDAR-independent manner and that MAPK/ERK and CREB are the downstream events of FAK activation. Further, FAK may interact with NR2A and NR2B to modulate LTP induction.

Animals↗
PubMed2002

Patterns of administration of antibody induction therapy and their associated outcomes.

1. There was a dramatic shift in the type of induction therapy used between 1996-2000. In 2000, more than half of recipients received induction therapy. 2. The type of transplants strongly influenced the use of antibody induction. LD recipients were least likely to receive antibody induction followed by unsensitized, sensitized cadaveric and SPK recipients. 3. Pan-T antibody induction was used more frequently in patients with DGF and in high immunologic risk groups. 4. IL-2 receptor antagonists have become the dominant induction therapy; even for recipients with high immunologic risk or those with DGF. 5. We cannot demonstrate the effects of pan-T antibody induction on the resolution of DGF. Pan-T antibody induction did not improve graft survival in any cohorts, although it was associated with lower acute rejection rates in LD and unsensitized groups. 6. IL-2R antibody induction therapy was associated with lower acute rejection and graft failure at one year in LD and unsensitized groups. However, this trend cannot be demonstrated in higher immunologic risk groups ie., sensitized cadaveric and SPK.

Adolescent↗
PubMed2004

[Role of phospho-calcium/ calmodulin-dependent protein kinase II in the induction and maintenance of long-term potentiation of C-fiber-evoked field potentials in spinal dorsal horn of the rat].

Our previous studies have shown that long-term potentiation (LTP) of C-fiber-evoked field potentials in the spinal dorsal horn is NMDA receptor dependent. It is known that elevation of Ca(2+) in the postsynaptic neurons through NMDA receptor channels during high-frequency stimulation of the afferent fibers is crucial for LTP induction, but how this leads to a prolonged potentiation of synaptic transmission in the spinal dorsal horn is not clear. In the hippocampus, a rise of Ca(2+) activates calcium/calmodulin-dependent protein kinase II (CaMK II) through autophosphorylation. Once this occurs, the kinase remains active, even when Ca(2+) concentration returns to baseline level. Phosphorylated CaMK II potentiates synaptic transmission by enhancement of AMPA receptor channel function via phosphorylation of GluR1 subunit of the receptor and the addition of AMPA receptors to synapses. Up to now, the role of CaMK II in the induction and maintenance of LTP of the C-fiber-evoked field potentials in spinal dorsal horn has not been evaluated. In the present study, we examined the expression of CaMK II and phospho-CaMK II in the lumbar segments (L4-L6) of the rat spinal dorsal horn at 30 min and 3 h after the establishment of LTP induced by tetanic electrical stimulation of the sciatic nerve (40 V, 0.5 ms pulses at 100 Hz for 1 s repeated four times at 10 s intervals) by using Western blot and electrophysiological techniques. To determine the role of the phospho-CaMK II in the induction and maintenance of the spinal LTP, a selective CaMK II inhibitor KN-93 (100 micromol/L) was applied directly onto the spinal cord at the recording segments before and after LTP induction. We found that (1) the protein level of phospho-CaMKII increased at both 30 min and 3 h after LTP induction, while the total protein level of CaMK II increased at 3 h but not at 30 min after LTP induction. (2) Spinal application of KN-93 at 30 min prior to the tetanus blocked both LTP induction and the increase in phospho-CaMK II. (3) 30 min after LTP induction, spinal application of KN-93 depressed LTP and the level of phospho-CaMK II (n=3). (4) Spinal application of KN-93 at 3 h after LTP, however, affected neither the amplitude of the spinal LTP nor the level of phospho-CaMK II in the spinal dorsal horn. These results suggest that activation of CaMK II is probably crucial for the induction and the early-phase maintenance of LTP of C-fiber-evoked field potentials in the spinal dorsal horn.

Animals↗
PubMed1990

The regulatory effects of cytokines on the induction of a peripheral immunologic tolerance in mice.

Previous reports have demonstrated that injection of rIL-1 alpha into mice abrogates the ability of deaggregated human gamma-globulin (HGG) to induce a state of antigen specific immunologic tolerance in vivo. Our results demonstrate that human rIL-1 beta and a bioactive nonapeptide of human IL-1 beta inhibit the induction of tolerance to HGG suggesting that IL-1 affects tolerance induction through a noninflammatory mechanism of action because the immunoactive nonapeptide possesses only immunomodulatory properties. Further, TNF-alpha but not IL-6, cytokines with many bioactivities in common with IL-1, was found to inhibit the induction of tolerance. Therefore, it appears unlikely that IL-6 plays a role in the pathway by which either IL-1 or TNF-alpha interferes with tolerance induction. Although IL-2, IL-4, and IFN-gamma were incapable of directly affecting the induction of tolerance to HGG, it was determined that IL-4 and IFN-gamma were capable of inhibiting the ability of IL-1 to abrogate tolerance induction. It has been suggested that IL-1 induces the generation of endogenous IL-1 in vivo. Further, it has been demonstrated that IFN-gamma as well as IL-4 inhibits the synthesis of IL-1. Inasmuch as IL-4 and IFN-gamma inhibit the ability of IL-1 to abrogate tolerance induction, it appears that it is the endogenously generated IL-1 that interferes with tolerance induction. It was also determined that neither IL-4 nor IFN-gamma inhibits the activity of IL-1 which is consistent with results reported by others. Thus, results presented here suggest that the inhibition of tolerance induction to HGG by IL-1 may involve the stimulation of endogenous IL-1 synthesis.

Amino Acid Sequence↗
PubMed1991

[Effects of rectal premedication and the mother's presence on induction of pediatric anesthesia].

The effects of the rectal premedication and the mother's presence on induction of anesthesia were studied with 67 children between the ages of 1 and 6 years. All children were induced with mask using nitrous oxide-oxygen-halothane. Children's emotional states during induction were categorized as excellent, good or fair. Rating of excellent or good was considered to indicate satisfactory induction. Forty-seven children were accompanied by their mother. Twenty-two of them were premedicated with rectal bromazepam (3 mg), while another twenty-five children were not premedicated. Satisfactory induction after premedication was performed on 78% of the 1-3 year olds and 100% of the 4-6 year olds, whereas without rectal premedication, satisfactory induction was achieved in 42% of the 1-3 year olds and 69% of the 4-6 year olds. Rectal premedication was important for satisfactory induction. Another twenty of all children were premedicated with rectal bromazepam (3 mg) and induced without mother presence. Satisfactory induction was performed on 38% of the 1-3 year olds and 100% of the 4-6 year olds. Mother's presence tended to lead to satisfactory induction. Furthermore, we sought feedback from the mothers about their presence during induction of anesthesia. Almost all of the mothers said they appreciated the opportunity to be present, with the exception of four mothers (8.5%) who reported feeling of some anxiety to be in an operating room.

Administration, Rectal↗
PubMed1988

Cytotoxicity and induction of sister chromatid exchanges in human and rodent brain tumor cells treated with alkylating chemotherapeutic agents.

Rodent (9L and 9L-2) and human (SF-126 and SF-188) brain tumor cells were treated with methylating, ethylating, and chloroethylating nitrosoureas. 9L-2 and SF-188 cells were 10-fold and 5.4-fold more resistant to the cytotoxic effects of 1-(2-chloroethyl)-1-nitrosourea (CNU) than were 9L and SF-126 cells. SF-188 cells were 2.5- to 3-fold more resistant to N-methyl-N-nitrosourea (MNU) and streptozotocin (STZ) than SF-126 cells. 9L-2 cells were slightly more resistant to the cytotoxic effects of STZ and MNU than were 9L cells, but the rodent cells were 5- to 15-fold more resistant to these agents than the human cells. There were only small differences in cytotoxicity among the four cell lines after treatment with N-ethyl-N-nitrosourea (ENU). SF-188 and 9L-2 cells were 7- to 8-fold more resistant to the induction of sister chromatid exchange (SCEs) by CNU than were SF-126 and 9L cells. SF-126 cells were 80-fold more sensitive to the induction of SCEs by both STZ and MNU than were SF-188 cells. Only small differences in SCE induction were observed in 9L and 9L-2 cells treated with MNU and STZ. After ENU treatment, SF-126, 9L, and 9L-2 cells showed similar levels of SCEs; SF-188 cells were more resistant to the induction of SCEs by ENU. Pretreatment of 9L-2 cells with MNU resulted in a dose-dependent increase in cytotoxicity and SCE induction by 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU). Treatment with 1 mM MNU completely reversed the cellular resistance of 9L-2 cells to BCNU but did not potentiate either cytotoxicity or SCE induction in 9L cells. These results suggest that O6-alkylguanine-DNA-alkyltransferase (O6-AT) plays an important role in determining the cytotoxicity of and the induction of SCEs by CNU in both rodent and human tumor cells. O6-AT may also influence the response of human cells to both the cytotoxic effects of and the induction of SCEs by MNU and STZ. In the rodent cells, however, biochemical mechanisms other than O6-AT appear to determine the cytotoxic response to these agents. O6-AT does not appear to influence the cytotoxicity of ENU in either human or rodent cells but may have a small effect on SCE induction in human cells.

Alkylating Agents↗
PubMed1984

Nerve growth factor-mediated enzyme induction in primary cultures of bovine adrenal chromaffin cells: specificity and level of regulation.

Primary cultures of bovine adrenal chromaffin cells provide large quantities of a homogeneous population of target cells for nerve growth factor (NGF) and, thus, are a suitable system for studying the molecular mechanism of action of NGF. In this study, we have shown that NGF mediates the specific induction of the key enzymes in catecholamine biosynthesis, tyrosine hydroxylase (TH), dopamine-beta-hydroxylase (DBH), and phenylethanolamine-N-methyltransferase (PNMT). Acetylcholinesterase (AChE), an enzyme which catalyzes the breakdown of acetylcholine, is also induced by NGF. We have compared NGF-mediated TH and AChE induction and have provided pharmacological evidence that TH induction involves a post-transcriptional, polyadenylation-dependent event (blockable by 9-beta-arabinofuranosyladenine but not by alpha-amanitin), whereas AChE induction requires transcription (blockable by alpha-amanitin). DBH and PNMT appear to be regulated via the same mechanism as TH. The time course of TH induction is such that NGF must be continuously present for at least the first 36 hr (during which time TH levels remain unchanged), and then the entire increase takes place during the subsequent 12 hr. In contrast, AChE induction proceeds linearly with time of NGF exposure. These data suggest that there may be multiple mechanisms by which NGF regulates enzyme induction. We have also compared the effects of cAMP with those of NGF. As compared to NGF, cAMP produces a different pattern of enzyme induction (in addition to TH, DBH, PNMT, and AChE, dopa decarboxylase (DDC) is also induced), it acts rapidly (a 12-hr exposure produces the full effect), and it acts only at the transcriptional level (its effects are blocked by alpha-amanitin). These data provide evidence that cAMP does not act as a second messenger for NGF with regard to enzyme induction.

Acetylcholinesterase↗
PubMed1994

A clinical trial of induction of labor versus expectant management in postterm pregnancy. The National Institute of Child Health and Human Development Network of Maternal-Fetal Medicine Units.

OBJECTIVE: Management of the uncomplicated pregnancy prolonged beyond the estimated date of confinement is controversial, particularly when the cervix is unfavorable for induction. The benefit of reducing potential fetal risk with induction of labor must be balanced against the morbidity associated with this procedure. The objective of this study was to compare two strategies for managing postterm pregnancy (i.e., immediate induction and expectant management). STUDY DESIGN: Four hundred forty patients with uncomplicated pregnancies at 41 weeks' gestation were randomized to either immediate induction of labor (n = 265) or expectant management (n = 175). Patients with expectant management underwent nonstress testing and amniotic fluid volume assessment twice per week. Patients in the induction group underwent induction within 24 hours of randomization. To evaluate the efficacy of intracervical prostaglandin E2 gel, patients in the induction group were randomized in a 2:1 scheme to receive either 0.5 mg prostaglandin E2 gel or placebo gel intracervically 12 hours before induction of labor with oxytocin. RESULTS: The incidence of adverse perinatal outcome (neonatal seizures, intracranial hemorrhage, the need for mechanical ventilation, or nerve injury) was 1.5% in the induction group and 1% in the expectant management group (p > 0.05). There were no fetal deaths in either group. There were no differences in mean birth weight or the frequency of macrosomia (birth weight > or = 4000 gm) between the two groups (p > 0.05). Regardless of parity, prostaglandin E2 intracervical gel was not more effective than placebo in ripening the cervix. The cesarean delivery rate was not significantly different in the expectant (18%), prostaglandin E2 gel (23%), or placebo gel (18%) groups. CONCLUSIONS: Adverse perinatal outcome in otherwise uncomplicated pregnancies of > or = 41 weeks is very low with either of the management schemes described. Thus from the perspective of perinatal morbidity or mortality either management scheme is acceptable.

Adult↗
PubMed1994

[Labor induction with prostaglandin in post-cesarean section status].

60 pregnant women with previous cesarean section and induction of labour with prostaglandins (PGE2) in the following pregnancy were compared to a collective of 1412 patients with PGE2 induction without any previous uterine surgery, and to a collective of 82 patients with previous cesarean section, but an uncomplicated course of pregnancy and therefore no indication for an induction of labour. Uterine hyperstimulation was more frequent in both collectives with previous cesarean section than in the collective without that risk. In the case of previous cesarean section induction of labour with prostaglandins did not lead to an increased number of uterine ruptures compared to cases with a previous cesarean section. Therefore the induction of labour itself in the case of a previous cesarean section doesn't lead to an increased maternal risk during delivery. Uterine hyperstimulation being rare, the increased number of fetal acidosis and vaginal-operative delivery in the group with previous cesarean section and consecutive PGE2 induction of labour seems to originate rather from the risk which was the indication for labour induction than from the PGE2 application itself. The information of a patient with previous cesarean section and planed induction of labour with PGE2 should therefore put the stress in the necessity of an intensive surveillance during delivery because of the basic risk "previous cesarean section" and the secondary risk resulting from the induction of labour.

Acidosis, Respiratory↗
PubMed1993

Regulation by bcl-2, c-myc, and p53 of susceptibility to induction of apoptosis by heat shock and cancer chemotherapy compounds in differentiation-competent and -defective myeloid leukemic cells.

Myeloid leukemias that differ in their competence for induction of differentiation were analyzed for expression of bcl-2 and c-myc and for their sensitivity to induction of apoptosis by heat shock and cancer chemotherapy compounds. The M1 leukemia expressed a high level of bcl-2 and showed a much lower susceptibility to induction of apoptosis by heat shock, Adriamycin, 1-beta-D-arabinofuranosylcytosine, methotrexate, and cycloheximide, compared to five other leukemias which expressed a low level of bcl-2. There was no association between susceptibility to induction of apoptosis and competence for induction of differentiation. The difference in susceptibility to methotrexate, which is not regulated by the multidrug resistance (MDR) genes, and treatment with verapamil, which blocks MDR activity, have indicated that the higher resistance of the M1 leukemia to these agents was not due to MDR activity. The results indicate that the level of regulated bcl-2 expression in these myeloid leukemias was associated with cell susceptibility to induction of apoptosis by different apoptosis-inducing agents. Screening for expression of bcl-2 may thus be useful to characterize leukemias regarding susceptibility to induction of apoptosis by different agents. The level of regulated c-myc expressed in these leukemias was not associated with susceptibility to induction of apoptosis. Transfection with a deregulated mutant p53 into the M1 leukemia did not change susceptibility to apoptosis induction, but transfection with deregulated c-myc increased susceptibility to apoptosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Antineoplastic Agents↗
PubMed1993

Induction of prophage lambda by nitrofurantoin and its modulation by butylated hydroxytoluene, sodium arsenite and alpha tocopherol.

Nitrofurantoin induced prophage-lambda in E. coli K12 strain GY5027(lambda) in a dose dependent manner, the maximum induction being 10-fold the spontaneous induction level and the maximum efficiency of induction 74%. The lever extract used as a metabolizing mixture enhanced the induction level significantly. Chloramphenicol at a concentration of 20 micrograms/ml inhibited the prophage induction by nitrofurantoin, indicating that the induction required concomitant protein synthesis. Butylated hydroxytoluene(BHT) and sodium arsenite enhanced the nitrofurantoin induced prophage-lambda induction in E. coli GY 5027(lambda) cells in a dose dependent manner. The maximum modulations in induction level (I/Io) were achieved with 100 micrograms/ml BHT and 250 micrograms/ml sodium arsenite corresponding to a nitrofurantoin concentration of 15 micrograms/ml and were found significant on statistical analysis. alpha-tocopherol, however, did not produce any effect on the prophage-lambda induction by nitrofurantoin.

Arsenic↗
PubMed1996

Stimulation of tissue-type plasminogen activator expression by retinoic acid in human endothelial cells requires retinoic acid receptor beta 2 induction.

We previously showed the involvement of retinoic acid receptor alpha (RAR alpha) in the induction of tissue-type plasminogen activator (t-PA) synthesis by RA in human umbilical vein endothelial cells (HUVECs). However, the rather slow onset of this induction of t-PA synthesis suggested an indirect role of RAR alpha. Here, we show that the protein synthesis inhibitor, cycloheximide completely blocks the induction of t-PA by RA, which points to the need of an intermediary protein in t-PA stimulation. This intermediary protein is likely to be RAR beta 2 on the basis of the following findings: (1) the induction of RAR beta by RA exactly precedes that of t-PA; (2) HUVECs with elevated RAR beta mRNA levels show an undelayed t-PA induction on stimulation with RA, and this response can be almost completely inhibited with an RAR antagonist; and (3) an antisense oligodeoxynucleotide against the translation initiation site of RAR beta 2 mRNA greatly reduces the t-PA induction by RA. Thus, induction of t-PA by RA in HUVECs involves a 2-step mechanism requiring induction of RAR beta 2 via RAR alpha, followed by induction of t-PA synthesis via RAR beta 2. Each of these steps is shown to have a different activation profile with RA and 9 cis RA.

Base Sequence↗