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At least 883 records · Page 49Linked to original sources
PubMed2006

Na(V)1.7 mutant A863P in erythromelalgia: effects of altered activation and steady-state inactivation on excitability of nociceptive dorsal root ganglion neurons.

Inherited erythromelalgia/erythermalgia (IEM) is a neuropathy characterized by pain and redness of the extremities that is triggered by warmth. IEM has been associated with missense mutations of the voltage-gated sodium channel Na(V)1.7, which is preferentially expressed in most nociceptive dorsal root ganglia (DRGs) and sympathetic ganglion neurons. Several mutations occur in cytoplasmic linkers of Na(V)1.7, with only two mutations in segment 4 (S4) and S6 of domain I. We report here a simplex case with an alanine 863 substitution by proline (A863P) in S5 of domain II of Na(V)1.7. The functional effect of A863P was investigated by voltage-clamp analysis in human embryonic kidney 293 cells and by current-clamp analysis to determine the effects of A863P on firing properties of small DRG neurons. Activation of mutant channels was shifted by -8 mV, whereas steady-state fast inactivation was shifted by +10 mV, compared with wild-type (WT) channels. There was a marked decrease in the rate of deactivation of mutant channels, and currents elicited by slow ramp depolarizations were 12 times larger than for WT. These results suggested that A863P could render DRG neurons hyperexcitable. We tested this hypothesis by studying properties of rat DRG neurons transfected with either A863P or WT channels. A863P depolarized resting potential of DRG neurons by +6 mV compared with WT channels, reduced the threshold for triggering single action potentials to 63% of that for WT channels, and increased firing frequency of neurons when stimulated with suprathreshold stimuli. Thus, A863P mutant channels produce hyperexcitability in DRG neurons, which contributes to the pathophysiology of IEM.

Action Potentials↗
PubMed2004

The role of calcium/calmodulin-dependent protein kinase II on the inactivation of MAP kinase and p34cdc2 kinase during fertilization and activation in pig oocytes.

The objective of this study was to investigate the role of calmodulin-dependent protein kinase II (CaMKII) during fertilization in the pig. Since it has been reported that CaMKII is involved in the capacitation and acrosome reaction of spermatozoa, we tested whether supplementation with the CaMKII inhibitor, KN-93, in the fertilization medium affected sperm penetration. The results showed that the addition of KN-93 in the fertilization medium significantly reduced the rate of sperm penetration into oocytes. However, pre-treatment with KN-93 before in vitro fertilization (i.v.f.) did not significantly affect sperm penetration, but it did affect pronuclear formation in a dose-dependent manner. In the oocytes pre-treated with KN-93 before i.v.f. and then co-cultured with spermatozoa without the drug, the decrease in p34cdc2 kinase and the cyclin B1 level were significantly suppressed as compared with those in penetrated oocytes without treatment with KN-93. However, the decrease in MAP kinase activity was not affected by KN-93. Additional treatment with KN-93 after Ca2+ ionophore treatment also inhibited the reduction in p34cdc2 kinase activity and the cyclin B1 level, but not MAP kinase activity. Treatment with KN-92, an inactive KN-93 analogue, did not significantly affect sperm penetration and pronuclear formation. In conclusion, the activation of CaMKII by artificial stimuli or sperm stimulated the disruption of cyclin B1 and the inactivation of p34cdc2 kinase, but did not affect MAP kinase inactivation during oocyte activation in pigs.

Animals↗
PubMed1983

[The effect of triphenyltin fluoride on aggregation, ATP secretion and malondialdehyde formation of rabbit platelets in vitro].

Recent studies have demonstrated that triphenyltin fluoride (TPTF), widely used as an agricultural chemical and a marine antifoulant, inhibits collagen-induced platelet aggregation and ATP secretion in rabbits ex vivo. The aim of the present investigation was to elucidate the mechanism of the inhibitory action of TPTF by investigating platelet malondialdehyde (MDA) formation, aggregation and ATP secretion following the stimulation by various stimuli of rabbit platelets treated in vitro with TPTF, other triphenyl metals and aspirin. Although no inhibitory effect of TPTF was found on sodium arachidonate-induced platelet aggregation and ATP secretion, TPTF inhibited dose-dependently both platelet aggregation and ATP secretion induced by collagen. The antiaggregating (IC50) concentration of TPTF was 6.0 X 10(-6) M against collagen. In addition, TPTF prevented the collagen-, and thrombin-induced formation of MDA, but had little inhibitory effect on the conversion of exogenous arachidonic acid to MDA in platelets. In contrast, aspirin (10(-3) M) inhibited platelet aggregation, ATP secretion and MDA formation induced by all the stimuli tested. Other triphenyl metals did not any inhibitory effect on collagen-, and sodium arachidonate-induced platelet aggregation and ATP secretion even at a final concentration at 10(-3) M. These results suggest that TPTF has a specific inhibitory effect on platelet aggregation and ATP secretion by acting at some step(s) of platelet membrane between the binding site of collagen and thrombin and the release of arachidonic acid.

Adenosine Triphosphate↗
PubMed2006

Characterization of the functional and growth properties of long-term cell cultures established from a human somatostatinoma.

In somatostatinoma, a rare malignant somatostatin (SST)-secreting neoplasia, tumour regression is rarely observed, implying the need for novel antiproliferative strategies. Here, we characterized a long-term culture (SST-secreting cancer (SS-C cells)) established from a human somatostatinoma. High concentrations of SST and chromogranin A were released by SS-C cells and SST release was stimulated by depolarizing stimuli and inhibited by the SST analogue, octreotide. SS-C cells expressed mRNA for SST receptor (SSTR) subtypes 1, 2 and 4, being also able to bind native SST. Moreover, SS-C cells were positively stained with an antibody to SSTR2. SS-C cells also expressed interferon-gamma (IFN-gamma) receptor mRNA and measurable telomerase activity. Our findings indicate that in vitro exposure of SS-C cells to native SST-28, to octreotide, to IFN-gamma, or to 3'-azido-3'deoxythymidine (AZT), a telomerase inhibitor, results in inhibition of SS-C cell proliferation. Concomitant with growth inhibition, apoptosis was detected in SST-, octreotide-, IFN-gamma- or AZT-treated SS-C cell cultures. Taken together our results characterized native SST, SST analogues, IFN-gamma and a telomerase inhibitor as growth-inhibiting and proapoptotic stimuli in cultured human somatostatinoma cells. Based on these findings, the potential of SST analogues, IFN-gamma and AZT, alone or in combination, should be further explored in the medical treatment of somatostatinoma.

Adult↗
PubMed1993

Intracochlear electrical tinnitus reduction.

Several reports have indicated that some cochlear implant patients experience a reduction in their tinnitus while listening to noise or speech. In the present study, two patients reporting bilateral tinnitus were selected from a group of adults with the Nucleus cochlear implant. They rated their tinnitus loudness and severity and completed the Tinnitus Handicap Questionnaire. The stimuli for electrical stimulation were charge-balanced pulse trains of various repetition rates (frequencies) and inter-electrode distances. A range of electrodes was chosen in each subject, including basal, medial and apical electrodes. For each condition, the hearing threshold level and the uncomfortable loudness level were determined. A range of stimulus levels between these two values were presented randomly. After each presentation, the patients rated the stimulus loudness and the tinnitus loudness on a 0 to 100 scale. These judgements were used to carefully determine the psychometric function between stimulus level and stimulus loudness, and between stimulus level and tinnitus loudness. All the parameters explored were important for maximizing the relationship between tinnitus reduction and stimulus loudness. First, the effectiveness of electrical stimulation in tinnitus reduction depended on the place along the cochlear partition. Second, a pulse rate of 125 Hz showed the greatest efficiency in terms of the current level needed to suppress tinnitus. Third, these two subjects showed rather poor performances in speech perception when using their speech processor in the usual condition and the hypothesis of an influence from tinnitus annoyance is suggested in addition to some more classical predicting factors of speech recognition in cochlear implant users.

Acoustic Stimulation↗
PubMed1994

Physiological identification of jaw-movement-related neurons in the trigeminal nucleus of cats.

Although neurons responsive to jaw movements have been identified in most parts of the trigeminal brainstem nuclei, little is known about how this information is relayed to the thalamus and ultimately to the cortex for kinesthetic functions and sensorimotor integration. The present extracellular recording experiments showed that a substantial amount of movement-related information is relayed to the thalamus through the caudal part of subnucleus interpolaris (Vi) in adult cats. Vertical jaw displacements, natural mechanical stimuli, and electrical stimulation of the masseter nerve were used to determine the receptive fields and response properties of movement-related neurons. Movement-related responses were observed in 161 units. The receptive fields of these units were located in the masseter muscle, other deep structures, hairy skin, oral mucosa, or some combination of these structures (i.e., convergent). The latency of units responding to masseter nerve stimulation ranged from 1.0 msec to 20 msec, which suggested that some movement-related information was provided by smaller-diameter muscle afferents. Movement responses were either tonic or phasic. Tonic units showed continuous firing at some jaw position; some of these showed a "dynamic" response to jaw displacement. Phasic units were only active, or showed increased activity, when the jaw moved through a specific position. Seventy-one movement-related units were activated by stimulation from the contralateral ventroposteromedial nucleus (VPM) of the thalamus. Most of the brainstem recording sites were located in the dorsal part of Vi between the caudal pole of the facial motor nucleus and the obex. Neurons in caudal Vi may be important for facial kinesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1996

A shear stress component to the modulation of capillary hydraulic conductivity (Lp).

OBJECTIVE: Two major factors that determine transcapillary exchange are Starling forces and hydraulic conductivity (Lp) of capillary walls. Although chemical stimuli alter Lp, the influence of mechanical stimuli has been neglected. Therefore, we tested the hypothesis that the Lp of intact capillaries would increase with the magnitude of changes in shear stress presented to each capillary. METHODS: Capillaries (n = 26) in the mesentery of pithed frogs (n = 23) were cannulated at 30 cm H2O (average in situ pressure = 9.2) to alter shear stress. For the calculation of shear stress, velocities of both frog red blood cells (RBC) and human RBC in the pipette solution were measured in each capillary before and after cannulation, respectively. Lp was assessed 2 min after cannulation. RESULTS: Venular capillaries only responded to the changes in shear stress. The magnitude of the changes in shear stress correlated positively with the values for capillary Lp (Kendall's tau = 0.56; p = 0.02). CONCLUSIONS: While Starling forces influence the movement of fluid by acting perpendicular to the long axis of capillaries, shear stress acts in a plane tangential to the capillary walls and appears to alter capillary Lp. In addition to chemical stimuli, the mechanical stimulation of capillaries can alter the barrier itself and consequently alter filtration rate.

Animals↗
PubMed2000

In vivo roles of integrins during leukocyte development and traffic: insights from the analysis of mice chimeric for alpha 5, alpha v, and alpha 4 integrins.

Mice chimeric for integrins alpha(5), alpha(V), or alpha(4) were used to dissect the in vivo roles of these adhesion receptors during leukocyte development and traffic. No major defects were observed in the development of lymphocytes, monocytes, or granulocytes or in the traffic of lymphocytes to different lymphoid organs in the absence of alpha(5) or alpha(V) integrins. However, in agreement with previous reports, the absence of alpha(4) integrins produced major defects in development of lymphoid and myeloid lineages and a specific defect in homing of lymphocytes to Peyer's patches. In contrast, the alpha(4) integrin subunit is not essential for localization of T lymphocytes into intraepithelial and lamina propria compartments in the gut, whereas one of the partners of alpha(4), the beta(7) chain, has been shown to be essential. However, alpha(4)-deficient T lymphocytes cannot migrate properly during the inflammatory response induced by thioglycolate injection into the peritoneum. Finally, in vitro proliferation and activation of lymphocytes deficient for alpha(5), alpha(V), or alpha(4) integrins upon stimulation with different stimuli were similar to those seen in controls. These results show that integrins play distinct roles during in vivo leukocyte development and traffic.

Animals↗
PubMed2002

Generation of biologically active angiostatin kringle 1-3 by activated human neutrophils.

The contribution of polymorphonuclear neutrophils (PMN) to host defense and natural immunity extends well beyond their traditional role as professional phagocytes. In this study, we demonstrate that upon stimulation with proinflammatory stimuli, human PMN release enzymatic activities that, in vitro, generate bioactive angiostatin fragments from purified plasminogen. We also provide evidence that these angiostatin-like fragments, comprising kringle domain 1 to kringle domain 3 (kringle 1-3) of plasminogen, are generated as a byproduct of the selective proteolytic activity of neutrophil-secreted elastase. Remarkably, affinity-purified angiostatin kringle 1-3 fragments generated by neutrophils inhibited basic fibroblast growth factor plus vascular endothelial growth factor-induced endothelial cell proliferation in vitro, and both vascular endothelial growth factor-induced angiogenesis in the matrigel plug assay and fibroblast growth factor-induced angiogenesis in the chick embryo chorioallantoic membrane assay, in vivo. These results represent the first demonstration that biologically active angiostatin-like fragments can be generated by inflammatory human neutrophils. Because angiostatin is a potent inhibitor of angiogenesis, tumor growth, and metastasis, the data suggest that activated PMN not only act as potent effectors of inflammation, but might also play a critical role in the inhibition of angiogenesis in inflammatory diseases and tumors, by generation of a potent anti-angiogenic molecule.

Angiostatins↗
PubMed1999

The NF-kappa B family member RelB is required for innate and adaptive immunity to Toxoplasma gondii.

The NF-kappa B family of transcription factors are associated with the regulation of innate and adaptive immunity to infection. Infection of C57BL/6 mice with Toxoplasma gondii resulted in up-regulation of NF-kappa B activity that included the NF-kappa B family member RelB. To assess the role of RelB in the regulation of the immune response to this infection, we challenged RelB-deficient mice (RelB-/-) and wild-type (WT) littermate controls with T. gondii. Although WT controls were resistant to T. gondii, RelB-/- mice succumbed 10-15 days after infection. Examination of accessory cell functions associated with resistance to T. gondii revealed that RelB-/- macrophages stimulated with IFN-gamma plus LPS or TNF-alpha produced IL-12 as well as reactive nitrogen intermediates and inhibited parasite replication similar to WT macrophages. Analysis of the systemic responses of RelB-/- and WT mice revealed that infected mice had similar serum levels of IL-12. However, RelB-/- mice challenged with T. gondii produced negligible levels of IFN-gamma and had reduced NK cell activity compared with WT mice. Similarly, splenocytes from uninfected RelB-/- mice stimulated with polyclonal stimuli were deficient in their ability to produce IFN-gamma. Together, our results demonstrate that RelB is essential for the development of innate NK and adaptive T cell responses that lead to the production of IFN-gamma and resistance to T. gondii.

Animals↗
PubMed1976

Functional significance of the ventral and lateral funiculi in the frog's spinal cord.

The spinal cord was transected at the level of calamus scriptorius either completely (spinal preparation) or partially (funicular preparation). In the operated frogs and in normal controls cranial and peripheral receptive fields were stimulated by natural stimuli. Results indicated that the information necessary for somatic activation of the protective flight ascends in the dorsolateral funiculus, which can be characterized as an ascending part of the reflex arc of somatotopically guided avoidance behavior. The tectal region is apparently a center of responses. The information necessary for activating different patterns of locomotion adequate to environmental conditions goes unilaterally through the ventral and ventrolateral funiculus. A diminished specificity of these motor patterns observed after injury of the ventrolateral funiculus seems to be related to a reduced feedback from the periphery. Lacking of aquatic pattern of limb movements (even when terrestrial patterns of locomotion were undisturbed), and drowning in water seem to be related to an injury of a vestibulo-spinal system in the ventral funiculus. It is concluded that the ventrolateral area of the frog spinal cord, i.e., the area between median fissure and dorsal root, forms a closed system providing afferent and efferent information sufficient to evoke normal behavior.

Animals↗
PubMed2000

Chondrocyte integrin expression and function.

The extracellular matrix (ECM) is an "information rich" environment and interactions between the chondrocyte and ECM regulate many biological processes important to cartilage homeostasis and repair including cell attachment, growth, differentiation, and survival. The integrin family of cell surface receptors appears to play a major role in mediating cell-matrix interactions that are important in regulating these processes. Chondrocytes have been found to express several members of the integrin family which can serve as receptors for fibronectin (alpha 5 beta 1), types II and VI collagen (alpha 1 beta 1, alpha 2 beta 1, alpha 10 beta 1), laminin (alpha 6 beta 1), and vitronectin and osteopontin (alpha V beta 3). Integrin expression can be regulated by growth factors including IGF-I and TGF-beta. By providing a link between the ECM and the cytoskeleton, integrins may be important transducers of mechanical stimuli. Integrin binding stimulates intracellular signaling which can affect gene expression and regulate chondrocyte function. Further studies are needed to more clearly define the role of integrins in cartilage.

Animals↗
PubMed1976

[The pressor reflex induced by skeletal muscle contraction and its influence on the reflex from the sino-aortic zones].

The cardiovascular response to 10 sec tetanic muscular contractions was studied in the decerebrated cat. A pressor reflex about 30 mm Hg occurred during hindlimb contractions evoked by ventral roots (L6, L7, S1) stimulation. The pressor reflex was associated with a decrease of blood flow in working and resting muscles and a minimal changes of heart rate and left ventricular contractility. An increase of systemic resistance, as a main cause of pressor reflex is suggested. Static contractions of muscles and stimulation of muscle nerve evoked stronger inhibition of baroreflex than cutaneous nerve stimulation of nociceptive stimuli. Inhibition of the cardiac component of baroreflex during muscular exercise was shown.

Animals↗
PubMed1976

[Determination of the latency for the prognosis of Bell's palsy (author's transl)].

In a previous study the authors discussed the value of the determination of the compound action potential amplitude of the m. orbicularis oris following supramaximal stimuli of the facial nerve for the prognosis of facial paresis. In this study they investigate the suitability of the determination of the latency periods for an early prognosis. The latency periods in 20 normal subjects and 26 patients with idiopathic facial paresis were messured and continuously checked. The study reveals that a difference of more than 0.5 msec. between the latency periods of normal and paretic patients does not even permit the proof of peripheral lesions in patients with partial denervation or absent or insufficient recovery. Ocassionally, even shorter latency were observed in paretic patients, which are probably due to a local increase of the threshold for supramaximal stimuli around the stimulation electrode. The necessary increase of the stimulus intensity probably leads to a nervous excitation further distally. Contrary to the observations of other authors these studies indicate that the determination of the latency does not constitute a useful prognostic criterion for idiopathic facial paresis; for an early prognosis the measurement of latency is less reliable than the determination of the compound action potential amplitude.

Electric Stimulation↗
PubMed2005

The oncoprotein I-2PP2A/SET negatively regulates the MEK/ERK pathway and cell proliferation.

I-2PP2A/SET, the translocation breakpoint-encoded protein expressed in acute undifferentiated leukemia, was identified as an inhibitor of protein phosphatase 2A (PP2A). Induction of exogenous I-2PP2A/SET at a ratio of 1:1 to the endogenous protein resulted in suppression of cell proliferation. In contrast, siRNA-mediated depletion of I-2PP2A/SET resulted in enhanced cell proliferation. Depletion of I-2PP2A/SET was accompanied with a decrease in the number of cells in G1 and an increase in cells in S phase. To examine the mode of action by which I-2PP2A/SET suppresses cell proliferation, we determined the effect of over-expressed I-2PP2A/SET on ERK activation. I-2PP2A/SET suppressed activation of ERK following EGF stimulation but did not affect activation levels of stress kinases, JNK and p38. By contrast, knocking down I-2PP2A/SET by siRNA resulted in enhancement of ERK and MEK activations, suggesting that I-2PP2A/SET negatively regulates MEK/ERK. These data suggest that I-2PP2A/SET negatively regulates cell growth by inhibiting the G1/S transition and inhibiting the MEK/ERK pathway stimulated by external stimuli. These data demonstrate that I-2PP2A/SET potentially functions as a tumor suppressor.

Cell Cycle↗
PubMed1991

[Early and late damage in bypass vessels induced by crystalloid and cardioplegic solutions].

Veins and arteries grafted into the aorto-to-coronary position undergo degenerative processes, subintimal fibrous hyperplasia and diffuse atherosclerosis. We examined the influence of various crystalloid and cardioplegic solutions on the endothelium of human saphenous veins and internal mammary arteries, bovine internal mammary veins and arteries and rabbit carotid arteries, using light microscopy, TEM, SEM, immunological techniques and quantitative permeability measuring methods. Immersion or perfusion of vessel segments for various periods of time led to an ultrastructural endothelial cell damage, to an increased endothelial permeability for macromolecules, partly to an endothelial cell loss. Addition of high concentrations of heparin impaired this effect. Under influence of various solutions an increased plaque development under stimulation with atherogenic stimuli was observed.

Animals↗
PubMed1991

Behavioural assessment of fetal health.

The assessment of behavioural activity of the fetus is widely used to assess fetal health in clinical practice as part of the biophysical profile as well as the nonstress test. Considerable information regarding normal activity patterns of healthy human fetuses have been obtained from 24 to 40 weeks gestation. It is this information which has provided the scientific foundation for the development of fetal assessment protocols. Studies in chronically-catheterized fetal sheep have demonstrated that acute hypoxemia leads to an inhibition of fetal breathing movements although prolonged reductions in oxygen delivery to the fetus in the absence of acidemia are associated with adaptation by the fetus and subsequent return to normal incidence of behavioural activity. The behavioural responses of the fetus to specific stimuli including vibroacoustic stimulation have been examined in relation to gestational age as well as type of stimulus, it is proposed that fetal acoustic stimulation could possibly be used to assess fetal neurological function although prior to it being accepted as an universal method for assessing fetal health it is essential that a greater understanding of the mechanisms involved in fetal responses to sound and vibration be determined using appropriate experimental techniques.

Behavior↗