Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.10.1 (ERK)
 95,504 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Promonocytic (U1) and T lymphocytic (ACH-2) cell lines chronically infected with human immunodeficiency virus type 1 (HIV-1) constitutively express low levels of virus, but expression can be induced by phorbol esters and cytokines. Whereas ACH-2 cells produce infectious virions, U1 cells produce defective, noninfectious particles. Although 3'-azido-3'-deoxythimidine (AZT) prevented acute HIV infection of susceptible cells, it did not prevent the induction of HIV expression in the infected cell lines. In contrast, interferon alpha (IFN-alpha) inhibited the release of reverse transcriptase and viral antigens into the culture supernatant after phorbol ester stimulation of both cell lines. Further, IFN-alpha suppressed the production or release (or both) of whole HIV virions, but had no effect on the amount of cell-associated viral proteins. Also, after phorbol ester stimulation of ACH-2 cells, IFN-alpha reduced the number of infectious viral particles secreted into the culture supernatant, but had no effect on the infectivity of cell-associated virus. These findings lend support to the combined use of antiviral agents that have action at both the early (AZT) and the late (IFN-alpha) stages of HIV replication.
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PMID:Interferon-alpha but not AZT suppresses HIV expression in chronically infected cell lines. 247 Jan 48

Thirty-five patients with active chronic hepatitis B (ACH-B) were evaluated. They were in stable replicative phase (HBeAg +; DNA polymerase and ALT stable in two determinations at least one month apart) and had not been infected by delta virus or HIV-1. Thirty-four patients were heterosexual and no patient was a drug abuser except one. The 23 initial cases were followed up for 15 months without therapy. The subsequent 12 cases were treated with maximal doses of 2.5 megaunits/m2 of lymphoblastoid alpha interferon (IFN-L) daily for two weeks and three times a week during 10 more weeks. While in the controls only two cases (8.69%) lost the DNA-polymerase activity and HBeAg, 5 treated patients (41.66%; p less than 0.05) developed seroconversion to nonreplicative phase. No patient from the control series lost the HBsAg; however, this happened in 2 treated patients (16.66%). These results show that IFN-L is effective in heterosexual patients with ACH-B in replicative phase without delta virus or HIV-I co-infection.
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PMID:[Treatment of chronic hepatitis B with lymphoblastoid alpha interferon]. 261 34

During the past decade, much has been learned about the pathophysiology of ACH--yet much remains to be determined. Although LC, IL-1, IL-2, IFN-gamma, and the T effector circuits have been extensively studied, it is still not clear whether it is LC- or keratinocyte-derived IL-1 that is crucial in ACH, whether IL-1 acts primarily on T-cells or the APC, whether other cytokines are involved in the circuit (TNF, KTGF?), the exact relationships between T effector, T memory, and other T helper cells, what the functions of mast cells and basophils are in the allergic reaction, and how the regulatory circuits (including prostaglandins and eicosanoids) affect the outcome of ACH. The mechanism of suppression remains even less well understood despite the potential application of this knowledge to the treatment of diseases caused by Type IV hypersensitivity. A better understanding of the ACH mechanism will lead not only to more sophisticated ACH treatment, but also to a better understanding of the cell-mediated events of cutaneous viral replication, organ transplantation, and tumor growth.
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PMID:The pathophysiology of allergic contact hypersensitivity. 269 Oct 41

Tumor necrosis factor alpha (TNF-alpha), also known as cachectin, was demonstrated to induce the expression of human immunodeficiency virus (HIV) in a chronically infected T-cell clone (ACH-2). Concentrations of recombinant TNF-alpha as low as 50 pg/ml induced a significant increase over background of HIV expression in the ACH-2 cells as determined by supernatant reverse transcriptase activity. The HIV-inducing effects of TNF-alpha could not be explained by toxic effects on the cells. In addition, both the uninfected parental cell line (A3.01) and the infected ACH-2 cells were shown to have high-affinity receptors for TNF-alpha. Transient-transfection experiments demonstrated that the inductive effects of TNF-alpha were due to specific activation of the HIV long terminal repeat. These studies provide evidence that TNF-alpha may play a role in the mechanisms of pathogenesis of HIV infection.
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PMID:Tumor necrosis factor alpha induces expression of human immunodeficiency virus in a chronically infected T-cell clone. 278 70

Oviducts of the salamander Ambystoma tigrinum contract in vitro in response to stimulation by arginine vasotocin (AVT) and acetylcholine (ACh). Steroid hormone pretreatment significantly affects the responsiveness of the oviductal tissue to AVT and ACh. Oviducts initially pretreated with estradiol, testosterone and saline or a combination of estradiol and testosterone exhibit no response to AVT and only saline or estradiol/testosterone treated oviducts respond to ACh. Secondary pretreatment with progesterone stimulated a significant increase in responsiveness to AVT and ACH in all groups.
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PMID:Response of amphibian (Ambystoma tigrinum) oviduct to arginine vasotocin and acetylcholine in vitro: influence of steroid hormone pretreatment in vivo. 285 37

The effect of taurine on the release of [3H]acetylcholine ([3H]ACH) and [3H]gamma-aminobutyric acid ([3H]GABA) from preloaded locust synaptosomes has been studied. Veratridine (100 microM) and K+ (100 mM) both evoked [3H]ACh release and this was reduced in a concentration-dependent manner by taurine (5, 10, and 20 mM). In contrast to this, veratridine induced no observable release of [3H]GABA, and the response to K+ was slight. In the presence of taurine, however, a concentration-dependent enhancement of [3H]GABA release was observed. Since nipecotic acid (1 mM), an inhibitor of neuronal GABA uptake, also revealed [3H]GABA release induced by veratridine, it is suggested that both this effect and that of taurine are due to prevention of GABA reuptake. These results suggest that taurine may act as a neuromodulator in insects.
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PMID:Effect of taurine on neurotransmitter release from insect synaptosomes. 290 94

The effect of Arg-atriopeptin III (ANP) on basal and stimulated (angiotensin II, acetylcholine and KCl depolarization) arginine vasopressin (AVP) release was characterized in the intact hypothalamo-neurohypophysial explant (HNS) and in isolated neurointermediate pituitary lobes (NIL). In initial experiments using 15-min incubation periods, ANP 10(-10) and 10(-9) M slightly inhibited basal AVP release in both NIL and HNS after a delay of at least 15 min. The most effective ANP concentration was 10(-10) M, and the inhibitory effect on AVP release was more marked in HNS (-52 +/- 5% of control compared to -29 +/- 8% for NIL). However, ANP 10(-10) M did not significantly attenuate KCl- or AII (10(-5) M)-stimulated AVP release from HNS after 15 min of exposure. When the incubation periods were increased to 30 min ANP 10(-10) and 10(-9) M significantly decreased AII-stimulated (10(-5) M) AVP release in a dose-dependent manner (p less than 0.05; p less than 0.01, respectively). The same concentrations of ANP did not significantly depress ACH-stimulated (10(-5) M) AVP release (p less than 0.1 for both concentrations). In summary, ANP generally inhibits AVP release in vitro by a slowly activated mechanism which appears to be specific for certain physiological stimuli. Although the site(s) of action cannot be absolutely localized to the ventral hypothalamus and/or the neurohypophysis, an effect in the hypothalamus seems very likely.
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PMID:In vitro evidence for an inhibitory effect of atrial natriuretic peptide on vasopressin release. 295 Mar 34

The K+ stimulated release of radioactively labelled ACH from cortical slices obtained from rats was increased by some pyridine derivatives that are metabolites of pyritinol. It appears that this effect is not mediated by an interaction with cholinergic receptors but may be related to the lipid solubility of the compounds. It is suggested that an effect of these metabolites on the membrane of nerve endings may be part of the mechanism by which pyritinol treatment increases ACH levels and release in old rats.
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PMID:Effects of some metabolites of pyritinol (Encephabol) on ACH release from brain slices. 321 29

We examined the role of the pressure natriuresis phenomenon in long-term arterial pressure control. Uninephrectomized dogs were housed in metabolic cages and made hypertensive with a continuous background intravenous infusion of angiotensin II (AngII, 12 ng/kg/min). To increase the ability of the kidney to excrete salt and water, we infused acetylcholine (ACH, 2.0 micrograms/kg/min), a potent natriuretic agen, directly into the renal artery. In four dogs, ACH decreased mean arterial pressure (MAP) from 144 +/- 5 mm Hg to 113 +/- 3 mm Hg. Sodium excretion increased by about 60% on the first day of infusion and then returned rapidly toward the control value. On cessation of the ACH infusion, there was a transient but marked sodium retention, and the hypertension returned. A control infusion of ACH intravenously rather than into the renal artery in the same four dogs did not affect MAP or sodium excretion during AngII hypertension.
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PMID:Hypotensive effect of chronic intrarenal infusion of acetylcholine during angiotensin hypertension. 337 Jan 36

For revealing the conjugation of impulse activity of simultaneously recorded neurones in the visual and sensorimotor areas of rabbits neocortex, histograms were built of cross- and autocorrelation (CCH and ACH) of their discharges sequences. From successions of discharges of the visual cortex neurones, forming pairs of cells acting in correlation, spikes were singled out conjugated with neuronal discharges in the sensorimotor area, and their ACHs were built. In 77% of cases a resemblance was observed of temporal structure of conjugated discharges and real spike sequences, in 23%--there was no such resemblance. Analysis of conjugated discharges ACHs showed that they appeared predominantly periodically (87% of cases). The number of fragments with periodic discharges frequency within delta-frequency range from 3 to 4 Hz prevailed.
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PMID:[Temporal structure of the spike trains of neuronal pairs in the neocortex during calm wakefulness in rabbits]. 337 71


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