Temperature sensitivity of cyclic adenosine 3':5'-monophosphate-binding proteins and the regulation of growth and differentiation in neuroblastoma cells. (57/267)

The apparent association constant (K-a) of cAMP to the binding proteins from resistant and nonresistant cells was 7.4 times 10-7 M-1 and 8.2 times 10-7 M-1, respectively, and the specific activity of cAMP BINDING TO THESE PROTEINS WAS SIMILAR FOR BOTH TYPES OF CELLS.  (+info)

Effects of dexamethasone and aminophylline on survival of Jurkat and HL-60 cells. (58/267)

The effects of dexamethasone and aminophylline on survival of Jurkat T-lymphocytic leukemia cells and HL-60 promyelocytic leukemia cells were investigated. Dexamethasone (10, 1000 nM) and aminophylline (1, 100 microM) induced apoptosis in Jurkat and HL-60 cells in a concentration-dependent manner. Treatment with a combination of dexamethasone (10 nM) and aminophylline (1 microM) significantly increased the number of apoptotic HL-60 cells, but not that of Jurkat cells, compared with dexamethasone (10 nM) or aminophylline (1 microM) treatment alone. Dexamethasone and aminophylline also increased the number of phospho-histone H2B (Ser(14))-positive Jurkat and HL-60 cells. Phospho-histone H2B (pH2B)-positive HL-60 cells were significantly increased by treatment with a combination of dexamethasone (10 nM) and aminophylline (1 microM), although no such effect was observed in Jurkat cells. On the other hand, simultaneous treatment with 10 nM dexamethasone and 1 muM aminophylline activated the 36-kDa MBP kinase, pro-apoptotic protein kinase in HL-60 cells. The activation of 36-kDa MBP kinase by dexamethasone and aminophylline was supported by studies showing an increase in the number of pH2B-positive and apoptotic Jurkat and HL-60 cells upon exposure to these drugs. Thus treatment with a combination of dexamethasone and aminophylline accelerates apoptosis of HL-60 cells via activation of 36-kDa MBP kinase and H2B phosphorylation.  (+info)

Responses to exogenous dibutyryl adenosine 3',5'-monophosphate of cardiac output and blood flow in the renal, superior mesenteric and carotid arteries in anesthetized dogs. (59/267)

Changes in the cardiac output and blood flow in the renal, superior mesenteric and carotid arteries in anesthetized dogs were observed, using the non-cannulating electromagnetic flow meter. Dibutyryl cyclic-AMP, 5 mg/kg body weight, was given intravenously and the following results were obtained: 1) Dibutyryl cyclic-AMP increased the stroke volume and the cardiac output, and slightly increased the heart rate. These effects appeared 3 to 5 min after administration of dibutyryl cyclic-AMP. 2) The mean systemic blood pressure as well as the central venous pressure fell slightly. 3) The renal and the superior mesenteric artery blood flow increased markedly, but the carotid artery blood flow did not change. 4) Distribution of the cardiac output to the renal and superior mesenteric arteries did not change but distribution to the carotid artery decreased. 5) Total peripheral resistance, renal artery vascular resistance and superior mesenteric artery vascular resistance decreased, and carotid artery vascular resistance decreased slightly. 6) The cardiac output and blood flow were enhanced by aminophylline (3 mg/kg), and were not blocked by propranolol (0.3 mg/kg).  (+info)

A survey of asthma mortality in patients between ages 35 and 64 in the Greater London hospitals in 1971. (60/267)

We have examined the death certificates from all patients aged 35-64 years who were recorded as dying from asthma in Greater London Council hospitals in 1971. Of the 47 death certificates studied, nine suggested that the primary cause of death was not asthma. From the remaining 38 deaths we have obtained 36 case records and found that 15 deaths occurred outside hospital and another two patients died in hospital having been admitted in a stable state. We have examined the remaining 19 case records to find out the circumstances of death in patients with asthma who die in hospital. We have been unable to exclude the possibility that many of the deaths in hospital were avoidable. Assessment of severity in most patients was incomplete, as judged by a retrospective analysis of case records, and many of the patients would be regarded as having had insufficient treatment. Four patients did not receive corticosteroids and in a further three the dose given was small. No physiological assessment of airflow obstruction was made in over half the patients. A comparison with 19 survivors of an admission to hospital with asthma did not provide enough information to account for the deaths. The survivors were in hospital for a shorter period of time, were slightly less ill, and were given comparable treatment regimens. Both groups of patients were inadequately assessed, and sedatives were given to approximately 70% of all subjects studied. The deaths in hospital usually occurred suddenly in the early morning in general medical wards.  (+info)

Evidence against an involvement of cyclic nucleotides in the induction of betacyanin synthesis by cytokinins. (61/267)

1. A wide range of purine bases, nucleosides and cyclic nucleotides were shown to induce betacyanin synthesis in Amaranthus seedlings. 2. The induction of pigment by benzyladenine, dibutyryl cyclic AMP or cyclic AMP was not potentiated by aminophylline. Aminophylline was shown to inhibit Amaranthus cyclic AMP phosphodiesterase activity. 4. Incubation of seedlings with aminophylline inhibited the conversion of 6-[G--3H]benzyladenine into presumed 9- and 7-glucosylbenzyladenine. 5. Induction of betacyanin synthesis by 6-benzyladenine or by exposure to red light was not accompanied by changes in the total cyclic AMP content in seedlings. 6. It is concluded that the inducers tested act as cytokinin analogues; no evidence was obtained to support cyclic AMP as an intermediate in the induction process.  (+info)

Influences of adenosine receptor antagonism on vasodilator responses to adenosine and exercise in adenosine responders and nonresponders. (62/267)

We previously demonstrated a bimodal distribution of vasodilator responsiveness to adenosine (Ado) infusion in human subjects, despite similar responses to exercise between subgroups [subjects responsive to Ado infusion (Ado responders) and subjects with blunted vasodilator responses to Ado infusion (Ado nonresponders]). (Martin EA, Nicholson WT, Eisenach JH, Charkoudian N, and Joyner MJ. J Appl Physiol 101: 492-499, 2006). A component of this difference was attributed to a larger nitric oxide component of Ado-mediated vasodilation in responders. However, there may also be differences in Ado receptors between these subgroups. We hypothesized that Ado receptor antagonism would reduce vasodilator responsiveness to Ado and exercise only in Ado responders. To test this hypothesis, we compared forearm vasodilation induced by intra-arterial infusion of three doses of Ado to vasodilation during three workloads of forearm handgrip exercise before and after Ado receptor antagonism with aminophylline (Aph) in 19 subjects. In Ado responders, the change in forearm vascular conductance above baseline for the low, medium, and high doses of Ado, respectively, was 93 +/- 16, 140 +/- 14, 194 +/- 18 before Aph and 27 +/- 12, 71 +/- 19, and 134 +/- 34 ml.min(-1).100 mmHg(-1) after Aph (P < 0.05 for low and medium dose before vs. after Aph). For nonresponders, these values were 30 +/- 5, 39 +/- 6, and 78 +/- 9 ml.min(-1).100 mmHg(-1) before Aph (P < 0.05 vs. responders), with no difference after Aph (P > 0.05). We found that Ado receptor blockade significantly inhibited exercise hyperemia only at high workloads in both responders and nonresponders (P < 0.05 before vs. after Aph). We conclude that there may be reduced Ado receptor responsiveness or sensitivity in nonresponders. Furthermore, Ado may play a limited role exercise hyperemia in both subgroups.  (+info)

The effects of cyclic N-2-O-dibutyryl- adenosine 3',5'-monophosphate, adrenaline and aminophylline on the isometric contractility of the isolated hemidiaphragm of the rat. (63/267)

1 N-2-O-dibutyryl adenosine 3',5'-monophosphate (db cyclic AMP), adrenaline and aminophylline produce a potentiation of the tension developed (Td) and the maximum rate of rise of tension (dT/dt max) in the rat isolated diaphragm during indirect electrical stimulation. Aminophylline and db cyclic AMP also produce the same effect during direct stimulation. 2 Propranolol produced a depression of the action of adrenaline on Td and dT/dt max during indirect stimulation of the diaphragm. On the other hand, the potentiating actions of db cyclic AMP and of aminophylline on Td and dT/dt max during indirect stimulation were unaffected by propranolol. 3 The results support the idea that cyclic AMP may be involved not only in regulating the processes associated with synthesis, mobilization and storage of transmitter in the motor nerve terminal, but also in modifying some metabolic processes which regulate the function of the contractile elements.  (+info)

Regulation of aryl hydrocarbon (benzo-(A)-pyrene) hydroxylase activity in mammalian cells. Induction of hydroxylase activity by N6,O2'-dibutyryl8 adenosine 3':5'-monophosphate and aminophylline. (64/267)

Treatment of hamster BHK cells with N6,O2'-dibutyryl adenosine 3':5'-monophosphate (Bt2cAMP), aminophylline, theophylline, or papaverine increased the level of aryl hydrocarbon (benzo(a)pyrene) hydrolxylase activity. The highese increase, 100-fold, was obtained with Bt2cAMP plus aminophylline or theophylline. N2,O2-Dibutyryl guanosine 3':5'-monophosphate gave a lower induction than Bt2cAMP. The level of hydroxylase activity started to decrease 6 hours after treatment with the inducer and was reduced to almost the uninduced level after 24 hours. Repeated addition of Bt2cAMP and aminophylline did not prevent this decrease. The hydroxylase can also be induced by treating cells with benz(a)anthracene, and the level of this induced activity was maintained for 24 hours. Aminophylline gave a 2- to 8-fold stimulation of the induction by benz(a)anthracene. The enzyme activity induced by Bt2cAMP, aminophylline, and benz(a)anthracene converted benzo(a)pyrene to similar alkali-extractable metabolities with a fluorescence spectra similar to that of 3-hydroxybenzo(a)pyrene. These induced enzyme activities also showed a similar heat stability. Induction by Bt2cAMP and aminophylline, like induction by benz(a)anthracene, required continued protein synthesis and only an initial period of RNA synthesis. Compared to the benz(a)anthracene-induced hydroxylase with a Km of 4.3 muM, the hydroxylase induced by Bt2cAMP and aminophylline showed a Km of 0.14 muM, and was 100-fold more sensitive to inhibition by 7,8-benzoflavone. Increasing the serum concentration in the culture medium stimulated the induction by aminophylline but did not stimulate induction by benz(a)anthracene. The results indicate that aryl hydrocaarbon (benzo(a)pyrene) hydroxylase can be induced by compounds that increase the level of adenosine 3':5'-monophosphate and that this induction and induced enzyme activity differs from that caused by benz(a)anthracene.  (+info)