Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.11.18 (MAP)
 7,412 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have characterized activation of the MAP kinase cascade in an inducible system in response to the temperature-sensitive (ts) expression of the v-mos oncogene. Transformation of immortalized rat embryo fibroblasts by a ts isolate of Moloney murine sarcoma virus (Mo-MuSVts110) constitutively activates MAP kinases (ERK-1 and ERK-2) and MAP kinase kinases (MKK-1 and MKK-2) only at the permissive temperature when v-mos kinase is present and active. Following a shift of the ts-transformed, serum-starved cells from the nonpermissive to permissive temperature, MAP kinases and both MKK-1 and MKK-2 are activated within 1-2 h, concurrent with the reappearance of active mos kinase. Raf-1 kinase activity increases more slowly in response to the reappearance of v-mos, and the mobility shift indicative of hyperphosphorylation was only detected 18 h after the temperature transition. Our data show that MAP kinase cascade activation is an early event following the reappearance of v-mos expression and v-mos kinase activity upon temperature shift, while the first manifestation of morphological transformation appears 24 h after the shift to permissive temperature. These results support the hypothesis that mos acts through the MKK to induce cell transformation.
Cell Growth Differ 1995 Sep
PMID:Activation of the mitogen-activated protein kinase cascade in response to the temperature inducible expression of v-mos kinase. 851 89

We report a case of transfusion-associated graft-versus-host disease (GVHD). A 79-year-old woman with Hodgkin's disease, respiratory failure and severe anemia who had been treated with two courses of chemotherapy was transfused with red cell concentrate (MAP-CRC) and fresh frozen plasma (FFP) in the ICU. On the 7-9th days after transfusion, she developed a diffuse erythematous rash mainly on the chest, high fever, liver dysfunction and thrombocytopenia. Despite treatment with immunoglobulin products and methylprednisolone, her condition deteriorated rapidly, and she died of multiple organ failure on the 7th day after appearance of rash. Skin biopsy demonstrated typical features of acute GVHD, suggesting that MAP-CRC-associated GVHD had occurred.
Masui 1995 Sep
PMID:[A case of graft-versus-host disease following red cell concentrate (MAP-CRC) transfusion]. 852 63

We developed a conscious, chronically instrumented, exercise-trained rat model and examined the time course of the training-induced alteration of baroreflex function in response to hypertensive conditions. Exercise-trained (ET) animals ran at 18 m.min-1, 15% grade, for 60 min.d-1, 5 d.wk-1 for 5 wk. Baroreflex tests were conducted on day 6 each week. Regression line slopes relating the change in mean arterial pressure (delta MAP) to the change in heart rate (delta HR) were used to assess baroreflex sensitivity. Intravenous injections of phenylephrine were used to create hypertensive conditions. Compared with the C group, slopes of ET animals were reduced (from 2.1 to 1.2 bpm.mm Hg-1, P < 0.05) as early as week 3 of training in response to increasing doses of PE, and reached 0.8 bpm.mm Hg-1 by the end of training. The reflex bradycardiac response (delta HR) to PE was reduced (P < 0.05) depending on the dose of PE and the duration of training: in micrograms PE.kg-1 body weight, 5 (71% +/- 6% of control at week 2), 3 (70% +/- 7% of control at week 3, and 1 (61% +/- 10% of control at week 4). The pressor (delta MAP) to PE remained constant throughout training. Thus, using a chronically instrumented rat model that maintains the ability to run, we observed that the ability of the arterial baroreflex to produce bradycardia during pressor events was substantially reduced following as few as 2 wk of training.
Med Sci Sports Exerc 1995 Sep
PMID:A chronically instrumented rat model to assess the altered baroreflex due to exercise. 853 35

Two groups of children, aged 1-4 years (n = 28) and 5-10 years (n = 28), respectively, received at random one of four doses of rocuronium (0.12, 0.17, 0.22 or 0.27 mg kg-1). When maximum block was obtained, further rocuronium to a total dose of 0.5 mg kg-1 was given. At a spontaneous T1 recovery of 25% the block was reversed with atropine and neostigmine in half the patients. The remainder were allowed to recover spontaneously. There was no difference in potency in the two age groups. An ED50 of 0.2 mg kg-1 was estimated. The estimates of ED50 were model-dependent of approximately 0.32 mg kg-1. The maximum block was found significantly higher in the younger age group (99.0 +/- 1.5% (mean +/- SD)) as compared to the older group (97.5 +/- 2.3%), and the clinical duration was also longer (16.6 +/- 5.3 min vs. 13.3 +/- 3.8 min), respectively. There was no significant difference between the two age groups in duration90 (26.9 +/- 6.5 min, 22.5 +/- 6.7 min, respectively) and duration0.7 (27.6 +/- 6.0 min, 24.9 +/- 7.9 min, respectively). Recovery time25-75, recovery time25-90, but not recovery time25-0.7 were found significantly longer in the 1-4 year group as compared to the times in older children. Neostigmine administration reduced recovery time by approximately half to two-thirds. MAP was not influenced by rocuronium. Following the injection of rocuronium in the younger age group there was a 15% increase in heart rate compared to a 10% increase in the age group 5-10 years.
Eur J Anaesthesiol Suppl 1995 Sep
PMID:Dose-response, time-course of action and recovery of rocuronium bromide in children during halothane anaesthesia. 855 11

The present study was designed to investigate the role of cardiopulmonary reflex, more specifically the Bezold-Jarisch reflex, in experimental hypertension induced by chronic administration of Nw-nitro-L-arginine methyl ester (L-NAME) (0.5 mg/ml) added to the drinking water for 6 days. The study was performed in male Wistar rats (200-350 g), 9 animals per group. L-NAME ingestion caused a significant increase in resting mean arterial pressure (MAP: 182 +/- 4 mmHg) and heart rate (HR: 447 +/- 20 bpm) when compared to untreated rats (MAP: 112 +/- 3 mmHg and HR: 355 +/- 10 bpm). Cardiopulmonary receptors were chemically stimulated with bolus injections of 5-hydroxytryptamine (5-HT, 4-10 micrograms/kg, iv) followed by measuring the falls in diastolic arterial pressure (DAP) and HR in conscious and freely moving animals. As expected, the responses to intravenous injections of 5-HT consisted of a dose-dependent reduction in HR (from 26 +/- 14 to 175 +/- 25 bpm) and DAP (from 7 +/- 4 to 39 +/- 3 mmHg) in the control rats. Both bradycardia and diastolic hypotension were significantly accentuated in the L-NAME animals (approximately 30%). These data suggest that, in contrast to other models of hypertension, in the present one caused by inhibition of nitric oxide synthesis, the Bezold-Jarisch reflex is exaggerated. This neural dysfunction could be related to changes in the cardiac vagal efferent or effector.
Braz J Med Biol Res 1995 Sep
PMID:Exaggerated Bezold-Jarisch reflex in the hypertension induced by inhibition of nitric oxide synthesis. 858 Aug 77

We studied in 13 hemodialysis patients intradialytic variations of blood volume (BV) and cardiac output, by means of non-invasive methods. We found a weak correlation, r 0.2 or less, between BV variations and intradialysis blood pressure variations. The sensitivity of the former in describing the variations of the latter was only 32%. During the 30 min preceeding the hypothensive crisis the percent BV variations did not show any predictive trend. On the contrary, refilling increased as blood pressure dropped and a weak inverse relation (r -0.35) was found between these two parameters. Unstable patients had predialytic blood volume values significantly lower than stable ones and comparable to healthy subjects. On the contrary, the correlation between percent variations of cardiac output index and MAP was 0.68 with a sensitivity and specificity of 90% and 59%, respectively. Unfortunately these promising results were obtained only with an estimate of cardiac output obtained by echocardiography and not by transthoracic impedance cardiography, which is much more feasible than the former as on-line monitoring of cardiac output. On-line monitoring of hemodynamic parameters is an appealing but still unsolved task.
Int J Artif Organs 1995 Sep
PMID:Non-invasive monitoring of hemodynamic parameters during hemodialysis. 858 65

Decreases in blood pressure are well known to increase the release of vasopressin. Studies were carried out to investigate whether vasopressin responses to postural changes in blood pressure are maintained in diabetic patients with orthostatic hypotension [DM-OH(+)] as well as non-diabetic patients with orthostatic hypotension [nonDM-OH(+)] and these responses were compared with those observed in normal subjects and diabetic patients without orthostatic hypotension [DM-OH(-)]. After 30 min in the supine position, the upright posture for 40 min was maintained and then the supine for 10 min. Blood pressure and heart rate (HR) were measured every 5 min and plasma vasopressin levels (plasma AVP) were determined every 10 min. In normal subjects and DM-OH(-), mean arterial blood pressure (MABP) did not change, but HR increased significantly by the upright position. Plasma AVP did not change in these groups. On the other hand, in DM-OH(+) MABP fell abruptly and remained to decrease during the upright posture. The HR responses in this group, however, were similar to those in normal control and DM-OH(-). Plasma AVP in DM-OH(+) significantly increased only at 30 min during upright. These increases were significantly greater than those in normal and DM-OH(-). There were significant correlation in changes in MABP (delta MAP) and plasma AVP (delta AVP) in DM-OH(+) (delta AVP = -0.13 MABP + 1.5, r = -0.32, p < 0.01). Relationship between delta MABP and delta AVP in nonDM-OH(+) was similar to that in DM-OH(+). It is concluded that AVP responses to orthostatic hypotension in diabetic and non-diabetic neuropathies were attenuated, but heart rate responses in these patients ware well reserved.
Tohoku J Exp Med 1995 Sep
PMID:Changes in plasma vasopressin levels and cardiovascular function due to postural changes in diabetic neuropathy. 869 86

It has been suggested that poliovirus (PV), the causative agent of poliomyelitis, could persist in surviving patients. We have previously shown that PV can persistently infect some human cell lines in vitro, particularly neuroblastoma cell lines. We report here an ex vivo model in which PV can persistently infect primary cultures of human fetal brain cells. Two mutations involving capsid residues 142 of VP2 and 95 of VP1 were repeatedly selected during the persistent infections. These residues are located in capsid regions known to be involved in interactions between PV and its receptor. During the first week after infection, viral antigens were found in cells of both the neuronal and glial lineages. In contrast, 2 weeks after infection, viral antigens were detected almost exclusively in cells of the neuronal lineage. They were detected predominantly in cells expressing a marker of early commitment to the neuronal lineage, MAP-5, particularly in neuroblasts. Viral antigens were also found in immature progenitors expressing a neuroepithelium marker, nestin, and in cells expressing a marker of postmitotic neurons, MAP-2. The presence of viral antigens in postmitotic neurons suggests that PV can persist in neurons of patients who have survived poliomyelitis.
J Virol 1996 Sep
PMID:Persistent poliovirus infection of human fetal brain cells. 870 69

Activation of several GTPases stimulates Na+-H+ exchange, resulting in an increased efflux of intracellular H+. These GTPases include alpha subunits of the heterotrimeric G proteins Gq and G13, as well as the low molecular weight GTP-binding proteins Ras, Cdc42, and Rho (Hooley, R., Yu, C.-Y., Simon, M., and Barber, D. L. (1996) J. Biol. Chem. 271, 6152-6158). GTPases coupled to the inhibition of Na+-H+ exchange, however, have not been identified. Several neurotransmitters, including somatostatin and dopamine, inhibit Na+-H+ exchange through a guanine-nucleotide-dependent mechanism, suggesting the involvement of a GTPase. In this study we determined that mutational activation of the alpha subunit of G12 inhibits the ubiquitously expressed Na+-H+ exchanger isoform, NHE1. Transient expression of mutationally activated Galpha12 inhibited serum- and Galpha13-stimulated NHE1 activity in HEK293 cells and CCL39 fibroblasts. In addition, in NHE-deficient AP1 cells stably expressing specific NHE isoforms, mutationally activated Galpha12 inhibited NHE1 activity but stimulated activities of the Na+-H+ exchanger (NHE) isoforms NHE2 and NHE3. In contrast, mutationally activated Galpha13, another member of the Galpha12/13 family, stimulated all three NHE isoforms. Although previous studies have identified a parallel action of Galpha12 and Galpha13 in regulating MAP (mitogen-activated protein) kinases and cell growth, these GTPases have opposing effects on NHE1 activity.
J Biol Chem 1996 Sep 13
PMID:Galpha12 differentially regulates Na+-H+ exchanger isoforms. 879 30

Our recent studies have implicated the TGF-alpha/epidermal growth factor receptor pathway in the genesis of testosterone (T) and estradiol-17 beta (E2)-induced dysplasia in the dorsolateral prostate (DLP) of Noble rats. This pathway was also found to be markedly up-regulated in the androgen-independent transplantable carcinoma that arose from the DLP of a Noble rat. In the current study, we investigated the expression of mitogen-activated protein kinase (MAP-kinase) and mitogen-activated kinase phosphatase-1 (MKP-1), key downstream regulators of growth factor-activated signal transduction in the DLP of castrated, castrated T-supplemented, and T+E2-treated rats and in the androgen-independent transplantable carcinoma. Both MAP-kinase and MKP-1 expression in the DLP were found to be dependent on androgen stimulation. Immunoblots of DLP from T+E2 treated rats demonstrated a selective decline in MKP-1 levels with no alteration in MAP-kinase expression. These findings suggest that the dual hormone treatment induces changes in the signal transduction pathway, which favors the protracted mitogenic action of MAP-kinase. In situ hybridization and immunohistochemistry findings corroborated the immunoblot data but also revealed that both MAP-kinase and MKP-1 were strongly expressed in severely dysplastic lesions, which may indicate the presence of transformed cells in these foci. In this regard, both proteins were strongly expressed in samples of the androgen-independent transplantable carcinoma. Taken together, results from this and our recent study suggest that alterations in a growth factor-MAP-kinase pathway may be important events in the initiation and progression of prostatic carcinoma.
Lab Invest 1996 Sep
PMID:Mitogen-activated protein kinase and mitogen-activated kinase phosphatase-1 expression in the Noble rat model of sex hormone-induced prostatic dysplasia and carcinoma. 880 59


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