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At least 37 records · Page 2Linked to original sources
PubMed1997

Functional activation of cerebral blood flow after cardiac arrest in rat.

After a period of global cerebral ischemia, CO2 reactivity and the hemodynamic-metabolic activation to functional stimulation are transiently suppressed. This raises the question of whether the impaired functional coupling reflects disturbances of functional integrity of the brain or an impaired cerebrovascular reactivity. We, therefore, compared the recovery of CO2 reactivity with that of somatosensory evoked potentials, functional flow activation and neurologic deficits in a rodent model of cardiac arrest-induced cerebral ischemia, followed by up to 7 days of reperfusion. Cardiac arrest of 10 minutes' duration was produced in 24 animals by electrical fibrillation of the heart. Five animals were sham-operated controls. Resuscitation was performed by external cardiac massage, using standard resuscitation procedures. Functional activation was carried out under chloralose anesthesia by electrical stimulation of forepaws. CO2 reactivity was tested by ventilation of animals with 6% CO2. During functional and hypercapnic stimulation CBF was measured in the somatosensory cortex using laser-Doppler flowmetry, and at the end of the experiment by 14C-iodoantipyrine autoradiography. Neurologic deficits were scored by evaluating consciousness and various sensory and motor functions. In control animals 6% CO2 increased CBF measured by laser-Doppler flowmetry by 28.8% +/- 8.7%. Forepaw stimulation generated somatosensory evoked potentials with an amplitude of 750 +/- 217 microV and increased CBF measured by laser-Doppler flowmetry by 86.0% +/- 18.1%. After return of spontaneous circulation, CO2 reactivity was transiently reduced to about 30% of control at 1 hour of reperfusion (P < 0.05) but returned to near control at 5 hours. Somatosensory evoked potential amplitudes were reduced to 15% of control at 45 minutes of reperfusion and returned to only 50% to 60% at 3 and 7 days after return of spontaneous circulation (P < 0.05). Functional activation of blood flow was completely suppressed during the first hour after return of spontaneous circulation but also recovered to 50% to 60% of control at 3 days after return of spontaneous circulation (P < 0.05). Linear regression analysis revealed a significant correlation between recovery of functional activation of blood flow and both recovery of the amplitude of somatosensory evoked potentials (P = 0.03) and the neurologic deficit score (P = 0.02), but not between neurologic deficit score and recovery of CO2 reactivity or somatosensory evoked potential amplitudes. These data demonstrate that the suppression of functional activation of blood flow after 10 minutes cardiac arrest is not related to impairment of coupling mechanisms but reflects ongoing disturbances of the functional integrity of the brain. Assessment of functional flow coupling is a reliable way to study postischemic recovery of the brain.

Animals↗
PubMed2005

The effect of total knee arthroplasty on joint movement during functional activities and joint range of motion with particular regard to higher flexion users.

PURPOSE: To evaluate active and functional knee excursion of patients before and after total knee arthroplasty (TKA) and to determine whether TKA restores quality of life related to functional activities of daily living. METHODS: Electrogoniometry was used to measure the functional movement of the knee during 11 activities of daily living in 50 patients who underwent TKA. These data were compared with the patient's active range of motion and quality-of-life scores. RESULTS: A cut-off point existed between loss and gain in flexion at between 90 and 95 degrees of preoperative active flexion. Two thirds of patients had preoperative flexion of more than 90 degrees, 83% of them had reduced flexion postoperatively. The remaining one third had preoperative flexion of 90 degrees or less, 85% of them had improved flexion postoperatively. A similar pattern of loss and gain occurred for functional movement of the knee. Reduced functional range was associated with significantly reduced physical quality of life compared with age-matched healthy subjects. CONCLUSION: Although TKA offers excellent pain relief and contributes to the overall well-being of the patient, these results suggest that it also leads to a reduced range of active and functional motion in the majority of patients. This is associated with a lower-than-normal physical quality of life. The design of implants and rehabilitation programmes should be reconsidered so that better range of motion and quality of life can be achieved for patients.

Activities of Daily Living↗
PubMed2005

Constructive feedforward neural networks using hermite polynomial activation functions.

In this paper, a constructive one-hidden-layer network is introduced where each hidden unit employs a polynomial function for its activation function that is different from other units. Specifically, both a structure level as well as a function level adaptation methodologies are utilized in constructing the network. The functional level adaptation scheme ensures that the "growing" or constructive network has different activation functions for each neuron such that the network may be able to capture the underlying input-output map more effectively. The activation functions considered consist of orthonormal Hermite polynomials. It is shown through extensive simulations that the proposed network yields improved performance when compared to networks having identical sigmoidal activation functions.

Algorithms↗
PubMed1988

Effect of heroin-conditioned auditory stimuli on cerebral functional activity in rats.

Cerebral functional activity was measured as changes in distribution of the free fatty acid [1-14C]octanoate in autoradiograms obtained from rats during brief presentation of a tone previously paired to infusions of heroin or saline. Rats were trained in groups of three consisting of one heroin self-administering animal and two animals receiving yoked infusions of heroin or saline. Behavioral experiments in separate groups of rats demonstrated that these training parameters imparts secondary reinforcing properties to the tone for animals self-administering heroin while the tone remains behaviorally neutral in yoked-infusion animals. The optical densities of thirty-seven brain regions were normalized to a relative index for comparisons between groups. Previous pairing of the tone to heroin infusions irrespective of behavior (yoked-heroin vs. yoked-saline groups) produced functional activity changes in fifteen brain areas. In addition, nineteen regional differences in octanoate labeling density were evident when comparison was made between animals previously trained to self-administer heroin to those receiving yoked-heroin infusions, while twelve differences were noted when comparisons were made between the yoked vehicle and self administration group. These functional activity changes are presumed related to the secondary reinforcing capacity of the tone acquired by association with heroin, and may identify neural substrates involved in auditory signalled conditioning of positive reinforcement to opiates.

Acoustic Stimulation↗
PubMed1999

STAT5b down-regulates peroxisome proliferator-activated receptor alpha transcription by inhibition of ligand-independent activation function region-1 trans-activation domain.

Growth hormone-activated STAT5b inhibits by up to 80% the transcriptional activity of peroxisome proliferator-activated receptor (PPAR) alpha, a nuclear receptor activated by diverse environmental chemicals and hypolipidemic drugs classified as peroxisome proliferators. This inhibitory cross-talk between STAT5b and PPAR is now reported for PPAR forms gamma and delta and for thyroid hormone receptor, indicating a more general potential for inhibitory cross-talk between JAK/STAT and nuclear receptor signaling pathways. Further investigations revealed that SOCS-3, a growth hormone-inducible negative regulator of cytokine signaling to STAT5b, abolished the STAT5b inhibitory response. A constitutively active STAT5b mutant failed to inhibit PPARalpha activity, indicating that STAT5b does not induce synthesis of a more proximal PPARalpha inhibitor. STAT5b inhibition was not reversed by overexpression of the heterodimerization partner of PPAR (retinoid X receptor) or the nuclear receptor coactivators P300 and SRC-1, suggesting that STAT5b does not inhibit PPARalpha by competing for these limiting cellular cofactors. STAT5b did not inhibit a chimeric receptor comprised of yeast GAL4 DNA-binding domain linked to the ligand binding/AF-2 trans-activation domain of PPARalpha, indicating that the COOH-terminal AF-2 domain of PPAR is not the target of STAT5b inhibition. Rather, STAT5b inhibited transcription driven by the NH(2)-terminal ligand-independent AF-1 trans-activation domain of PPARalpha in a GAL4-linked chimera by approximately 80%. The conservation of this AF-1 trans-activation function in many nuclear receptors suggests that AF-1 may serve as an important target for inhibitory cross-talk between STAT transcription factors and nuclear receptors in a variety of signaling pathways.

Animals↗
PubMedDate not supplied

[Role of norepinephrine in the regulation of thyroid gland functional activity in rabbits].

By collecting in situ the blood flowing from the thyroid, the authors have demonstrated that noradrenaline injected in a dose 1 microgram/kg into rabbit thyroid artery enhanced triiodothyronine secretion without changing thyroxin secretion. This process was inhibited by prazosin, an alpha-adrenoblocker, in a dose 1 microgram/kg, injected 5 min before noradrenaline, but not by propranolol, a beta-adrenoblocker. Phenylephrine, an alpha-adrenergic agonist, in a dose 1 microgram/kg, injected into the thyroid artery, influenced thyroid hormone secretion similarly as noradrenaline. The T3/T4.100 ratio taken as an indicator of T4 thyroid conversion increased under the effect of noradrenaline injection after prazosin. Thus, in our experiment noradrenaline activated thyroid function via stimulation of alpha-adrenoceptor system. Hence, catecholamines are capable of directly influencing thyroid functional activity.

Animals↗
PubMed1990

The leukocyte integrin LFA-1 reconstituted by cDNA transfection in a nonhematopoietic cell line is functionally active and not transiently regulated.

The functional activity of lymphocyte function-associated antigen 1 (LFA-1) on leukocytes can be regulated by T-cell receptor (TCR) stimulation and pharmacologic agents. It was of interest to determine if functionally active LFA-1 could be reconstituted on a nonhematopoietic, LFA-1-negative cell line. We report the expression of LFA-1 and diethylaminoethyl (DEAE) Mac-1 alpha beta heterodimers on the cell surface of a fibroblastoid cell line, COS, by DEAE dextran cotransfection of the alpha and beta subunit cDNAs. Immunoprecipitation studies demonstrated that the alpha and beta subunit was expressed in heterodimers. The alpha or beta subunit was expressed at lower levels after transfection with the alpha or beta subunit cDNA alone. Cotransfection of the alpha and beta subunit cDNAs, but not transfection of alpha or beta alone, was sufficient to reconstitute intercellular adhesion molecule-1 (ICAM-1) binding activity. Consistent with this observation, LFA-1 on the fibroblastoid cells possesses the activation epitope defined by the L16 monoclonal antibody (mAb). This epitope marks the conversion of LFA-1 from the low to high avidity state on peripheral blood T lymphocytes (PBLs) and is constitutively present on activated cell lines. In contrast to LFA-1 on leukocytes, the functional activity of LFA-1 on fibroblastoid cells was not influenced by phorbol ester treatment. Furthermore, the use of agents that interfere with intracellular signaling, a protein kinase C inhibitor, cAMP analogue, or the combination of a phosphodiesterase inhibitor and adenyl cyclase activator, did not affect the binding of COS cells expressing LFA-1 to purified ICAM-1.

Alkaloids↗
PubMed1994

Clinical significance of neutrophil functional activity in HIV infection.

Functional activity of polymorphonuclear neutrophils (PMN) was tested in 63 HIV-1 infected patients. PMN chemiluminescence (CL) and intracellular enzyme activity were both depressed in patients at all stages of infection, though this depression was more pronounced in AIDS patients. We found no such depression when cells were incubated in the presence of autologous serum. PMN phagocytosis in the presence of serum was reduced in the early stage of HIV infection (LAS) but was in the normal range in AIDS patients. No differences in PMN functional activity between patients with LAS and those with dermatological disorders were found. The appearance of recurrent upper respiratory tract infection was associated with reduced PMN CL. The most pronounced changes in PMN activity were observed in patients with severe, recurrent bacterial pneumonia and Pneumocystis carinii pneumonia. A lower level of PMN activity was found in patients with infection progressing rapidly towards AIDS than in patients with a relatively stable course of infection. Thus, PMN CL may be regarded as a predictive factor for the progression of HIV infection.

AIDS-Related Opportunistic Infections↗
PubMedDate not supplied

[Antibody functional activity in immunization with influenza vaccines].

The functional activity of serum antibody had been shown previously to reflect the state of resistance to influenza more accurately than antibody concentration. The functional activity of antibodies in the vaccination process was studied. The immune response to influenza antigens was found to be accompanied by an increase in the functional activity of antibodies, the intensity of this increase was the highest in natural influenza infection, moderate after administration of live vaccines and the least after immunization with inactivated preparations. The vaccine strains may differ significantly in their capacity to stimulate antibody with high functional activity. The quantitative parameters of the functional activity of antibody are directly related to the antigen dose and frequency of antigenic stimulation.

Adult↗
PubMed1993

Modulators of cellular protein phosphorylation alter the trans-activation function of human progesterone receptor and the biological activity of progesterone antagonists.

Addition of progesterone to breast cancer cells in vivo increases phosphorylation of human progesterone receptor (PR), suggesting that phosphorylation has a regulatory role in producing the activated form of receptor. Kinetic analysis indicates that hormone-dependent phosphorylation is sequential and that early stages of phosphorylation(s) are closely associated with enhancement of PR-DNA binding while later stages are associated with a trans-activation function. Various agents that stimulate cellular protein phosphorylation (8-Br cAMP, okadaic acid, TPA) functionally synergize with progesterone to enhance progesterone-dependent PR trans-activation in intact cells. These results suggest that protein phosphorylation does have a role in modulating the trans-activation function of PR in vivo. They also demonstrate cross-talk between second messenger signal transduction pathways and nuclear steroid receptors. Whether the phosphorylated target that provides the link between these two signal transduction pathways is PR itself or another protein involved in PR-mediated gene transcription is not known. Positive cooperative interactions were also observed between cAMP signaling pathways and the progesterone antagonist RU486, that resulted in RU486 exerting substantial agonist activities. This ability of cross-talk between second messenger and steroid receptor signal transduction pathways to override the antagonistic effects of RU486 suggests a novel mechanism to explain the problem of resistance to clinically important steroid antagonists.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2002

Transcription activation by FNR: evidence for a functional activating region 2.

The FNR protein of Escherichia coli controls the transcription of target genes in response to anoxia via the assembly-disassembly of oxygen-labile iron-sulfur clusters. Previous work identified patches of surface-exposed amino acids (designated activating regions 1 and 3 [AR1 and AR3, respectively]) of FNR which allow it to communicate with RNA polymerase (RNAP) and thereby activate transcription. Previously it was thought that FNR lacks a functional activating region 2 (AR2), although selecting for mutations that compensate for defective AR1 or a miscoordinated iron-sulfur cluster can reactivate AR2. Here we show that the substitution of two surface-exposed lysine residues (Lys49 and Lys50) of FNR impaired transcription from class II (FNR box centered at -41.5) but not class I (FNR box centered at -71.5) FNR-dependent promoters. The degree of impairment was greater when a negatively charged residue (Glu) replaced either Lys49 or Lys50 than when uncharged amino acid Ala was substituted. Oriented heterodimers were used to show that only the downstream subunit of the FNR dimer was affected by the Lys-->Ala substitutions at a class II promoter. Site-directed mutagenesis of a negatively charged patch ((162)EEDE(165)) within the N-terminal domain of the RNAP alpha subunit that interacts with the positively charged AR2 of the cyclic AMP receptor protein suggested that Lys49 and Lys50 of FNR interact with this region of the alpha subunit of RNAP. Thus, it was suggested that Lys49 and Lys50 form part of a functional AR2 in FNR.

Amino Acid Substitution↗
PubMed2005

Functional activity of mitochondrial nitric oxide synthase.

The functional activity of mitochondrial nitric oxide synthase (mtNOS) is determined by inhibiting O2 uptake and by enhancing H2O2 production. The effect of mtNOS activity on mitochondrial O2 uptake is assayed in state 3 respiration in two limit conditions of intramitochondrial NO: at its maximal and minimal levels. The first condition is achieved by supplementation with L-arginine and superoxide dismutase (SOD), and the second by addition of an NOS inhibitor and oxyhemoglobin. The difference between state 3 O2 uptake in both conditions constitutes the mtNOS functional activity in the inhibition of cytochrome oxidase activity. The functional activity of mtNOS in enhancing mitochondrial H2O2 generation in state 4 is given by the NO inhibition of ubiquinol-cytochrome c reductase activity. Simple determinations with the oxygen electrode or the measurement of mitochondrial H2O2 production can be used to assay the effects of physiological and pharmacological treatments on mtNOS activity.

Animals↗
PubMed1987

Adenovirus transforming 19-kD T antigen has an enhancer-dependent trans-activation function and relieves enhancer repression mediated by viral and cellular genes.

The adenovirus E1b region codes for two major tumor antigens of 19 kD and 55 kD, which are important for cell transformation. Our results indicate that the 19-kD T antigen possesses two enhancer-regulatory functions. It can trans-activate enhancer-linked promoters and relieve enhancer repression mediated by viral and cellular repressors. The 19-kD activation function enhances expression from different promoters linked to SV40, Py, Ela, and immunoglobulin heavy-chain enhancers. Enhancer activation by the 19-kD protein appears to be cell type-specific, since the heavy-chain and SV40 enhancers were not trans-activated in myeloma cells whereas the same enhancers were trans-activated in fibroblasts. The 19-kD enhancer activation function appears to be dominant over the enhancer repression function of E1a, since in cells expressing the 19-kD protein there is no significant repression despite a large increase in E1a expression. The 19-kD T antigen activates the Py enhancer in undifferentiated F9 cells indicating that the activation function of E1b masks enhancer repression by an "E1a-like" cellular gene product. The enhancer activation function of the 19-kD T antigen may be important for cell transformation and cell differentiation.

Adenovirus Early Proteins↗
PubMed2004

Effects of secretory products of activated neutrophils on morphological composition and functional activity of peritoneal exudation cells during inflammation of staphylococcal origin.

Substance A5 isolated from supernatants of activated neutrophils from donors significantly increases the percentage of neutrophils and macrophages in the peritoneal exudation of mice on days 3 and 7 of staphylococcal inflammation and stimulates functional activity (lysosomal, phagocytic, and NBT-reducing) of these cells, reduced as a result of inflammation, on days 3, 7, and 14 of the inflammatory process.

Animals↗
PubMed1992

Density of perfused capillaries in living human brain during functional activation.

Recent evidence has indicated that functional activation of cerebral cortex is accompanied by increases of blood flow and glucose consumption but not oxygen consumption. No explanation has been advanced for this change of the flow-metabolism couple. We formulated the hypothesis that oxygen delivery to brain tissue is diffusion-limited by the enormous hemoglobin binding, and rate-limiting for the oxygen consumption of the tissue. One prediction of this hypothesis is very low oxygen tensions in the tissue. A second prediction is the inability of oxygen consumption to increase during functional activation in the absence of recruitment of capillaries for the oxygen diffusion capacity. We designed a study to test the latter prediction by calculating the density of functioning capillaries during vibrotactile stimulation of the parietal cortex. We defined functioning capillaries as capillaries that transport glucose and therefore calculated the capillary density from the glucose diffusion capacity (K1) of the cerebral capillaries. We confirmed the presence of a partial flow-CMRglc couple (2:1) during the functional activation. Oxygen consumption did not change despite an increase of capillary density in proportion to the change of blood flow.

Brain↗
PubMed1999

Activity of the Nurr1 carboxyl-terminal domain depends on cell type and integrity of the activation function 2.

Nurr1, a member of the nuclear hormone receptor superfamily, was recently demonstrated to be of critical importance in the developing central nervous system, where it is required for the generation of midbrain dopamine cells. Nuclear receptors encompass a transcriptional activation function (activation function 2; AF2) within their carboxyl-terminal domains important for ligand-induced transcriptional activation. Since a Nurr1 ligand remains to be identified, the role of the Nurr1 AF2 region in transcriptional activation is unclear. However, here we show that the Nurr1 AF2 contributes to constitutive activation independent of exogenously added ligands in human embryo kidney 293 cells and in neural cell lines. Extensive mutagenesis indicated a crucial role of the AF2 core region for transactivation but also identified unique features differing from previously characterized receptors. In addition, Nurr1 did not appear to interact with, and was not stimulated by, several previously identified coactivators such as the steroid receptor coactivator 1. In contrast, adenovirus protein E1A, stably expressed in 293 cells, was shown to contribute to AF2-dependent activation. Finally, while the AF2 core of RXR is required for ligand-induced transcriptional activation by Nurr1-RXR heterodimers, the functional integrity of Nurr1 AF2 core is not critical. These results establish that the ligand binding domain of Nurr1 has intrinsic capacity for transcriptional activation depending on cell type and mode of DNA binding. Furthermore, these results are consistent with the possibility that gene expression in the central nervous system can be modulated by an as yet unidentified ligand interacting with the ligand binding domain of Nurr1.

Adenovirus E1A Proteins↗