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At least 523 records · Page 29Linked to original sources
PubMed1987

Regulation of low density lipoprotein receptor gene expression in cultured human granulosa cells: roles of human chorionic gonadotropin, 8-bromo-3',5'-cyclic adenosine monophosphate, and protein synthesis.

Treatment of human granulosa cells with human CG (hCG) or an analog of its second messenger, cAMP, promotes a rapid increase in low density lipoprotein (LDL) receptor mRNA content. After 1 h of treatment with 8-bromo-cAMP, an appreciable increase in hybridizable LDL receptor mRNA was found which increased to apparently maximal levels within 4-6 h. Treatment of the granulosa cells with 25-hydroxycholesterol, in the presence of aminoglutethimide, resulted in a reduction in LDL receptor mRNA content within 6 h of treatment. However, hCG or 8-bromo-cAMP were able to stimulate an increase in LDL receptor mRNA content in the presence of this inhibitory signal. We further investigated the mechanism by which tropic agents increased mRNA content. While inhibition of RNA synthesis with actinomycin D blocked the hCG or cAMP-induced rise in LDL receptor mRNA content, inhibition of protein synthesis with cycloheximide augmented basal or hCG- or cAMP-stimulated LDL receptor mRNA levels. We conclude that human steroidogenic cells possess a cAMP-mediated mechanism for rapid upregulation of LDL receptor mRNA which is distinct from, and supercedes, cholesterol negative feedback of LDL receptor gene expression. The actions of hCG and 8-bromo-cAMP do not require ongoing protein synthesis. Indeed, a cycloheximide-sensitive mechanism modulates receptor mRNA levels in these cells such that the effects of hCG and 8-bromo-cAMP are enhanced when cells are pretreated with this drug.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1989

Characteristics of human synovial fibroblast activation by IL-1 beta and TNF alpha.

Human synovial fibroblast cell lines (HSN), established from tissues obtained from the knee joints of arthritis patients undergoing arthoplasty, were used to investigate the effects of human interleukin-1 (IL-1) beta and tumour necrosis factor (TNF)alpha on proliferation and prostaglandin E2 (PGE2) secretion. IL-1 beta and TNF alpha were equipotent stimulators of HSN proliferation. Classical non-steroidal anti-inflammatory drugs and glucocorticoids significantly augmented this effect. In addition, IL-1 beta and TNF alpha were potent inducers of PGE2 production while exogenous PGE2 was growth inhibiting. These data suggest that the secretion of PGE2 by monokine-stimulated HSN exerts a negative feedback signal. Further examination of IL-1 beta- and TNF alpha-induced PGE2 secretion revealed IL-1 beta to be a more potent stimulator; however, this observation may be due, in part, to differences in the kinetics of induction. Rabbit anti-IL-1 beta and anti-TNF alpha specifically neutralized both proliferation and PGE2 production induced by these monokines, but anti-IL-1 beta (or anti-IL-1 alpha) did not block TNF alpha activity. It is unclear whether TNF alpha stimulates HSN to produce IL-1, but the antibody data suggest that extracellular IL-1 is not responsible for TNF alpha in vitro activity.

Cell Division↗
PubMed1990

Effect of angiotensin and other pressor agents on tubuloglomerular feedback responses.

Experiments were performed in anesthetized rats to examine the effect of an intravenous infusion of norepinephrine or vasopressin on the tubuloglomerular feedback (TGF) response of stop flow pressure (PSF). During infusion of norepinephrine at an average rate of 107.5 ng/kg min, mean femoral arterial pressure (MAP) increased from 102.1 +/- 3.55 to 113.7 +/- 3.44 mm Hg and PSF-max increased from 7.45 +/- 1.13 to 9.95 +/- 1.19 mm Hg. When MAP was returned to control by a suprarenal aortic clamp PSF-max was 5.64 +/- 1.09 mm Hg (NS vs. control). Similarly, at an infusion rate of 226.5 ng/kg min PSF-max was not significantly different from control (6.79 +/- 1.61 mm Hg). V1/2, the half-maximum flow rate, was not altered by norepinephrine whether MAP increased or was kept constant. Infusion of vasopressin at the pressor dose of 13.0 mU/kg min increased MAP by about 25 mm Hg and raised PSF-max from 6.56 +/- 0.84 to 14.45 +/- 1.54 mm Hg. However, when MAP was returned to normal PSF-max was 5.41 +/- 0.75 mm Hg (NS). Our data show that in contrast to angiotensin II, norepinephrine and vasopressin do not augment TGF responses when a rise in MAP is prevented. Angiotensin II appears to play a specific role in altering the sensitivity of the TGF mechanism.

Angiotensin II↗
PubMed1996

Increased tubular flow induces resetting of tubuloglomerular feedback in euvolemic rats.

As single-nephron glomerular filtration rate (SNGFR) and late proximal flow (VLP) increase during growth or following volume expansion, the tubuloglomerular feedback (TGF) function (defined as the decrement in SNGFR due to the process of TGF) shifts rightward in the plane defined by VLP and SNGFR as required to maintain the homeostatic efficiency of TGF. It is not known whether this resetting of TGF requires changes in the systemic hormonal milieu or results from prolonged activation of TGF itself. We employed micropuncture and videometric flow velocitometry (an optical technique for measuring flow in unobstructed nephrons) to address this issue in Inactin-anesthetized euvolemic rats. The fractional compensation (C) of TGF for perturbations [late proximal flow perturbation (VH) = +/- 5 nl/min] in VLP was assessed repeatedly before and during a sustained increase in flow imposed by adding 20 nl/min to early proximal flow (VEP). Augmenting VEP initially saturated TGF, thus suppressing C. Over the next 30 min, C recovered to 70% of its original value, suggesting a rightward resetting of the TGF function to match the increase imposed on VLP. Resetting was confirmed by documenting an evolving asymmetry of C about VH = 0 by testing C vs. VH for -12 < or = VH < or = 12 in increments of 4 nl/min. Beyond 30 min of augmented VEP, C gradually declined due to desensitization of TGF. A sustained increase in VLP is sufficient to include TGF resetting, independent of any change in the systemic neurohumoral milieu.

Animals↗
PubMedDate not supplied

Cineplasty as a control input for externally powered prosthetic components.

To achieve significant improvement in the function of electric-powered, upper-limb prostheses, we believe it is necessary to develop better control interfaces with inherent sensory feedback. Small cineplasties, or other surgical procedures that also externalize the force and excursion of a muscle, could potentially provide this superior control. Connecting a muscle to a prosthetic component via a controller that embodies the concept of extended physiological proprioception (EPP) would enable the physiological sensory feedback inherent in the skin, muscle, and other tissues of the cineplasty to inform the user of the state of the prosthesis. Multiple miniature forearm tunnel cineplasties, each with an EPP controller, might enable meaningful independent multifinger control of hand prostheses. At higher levels of amputation (e.g., transhumeral), small pectoral or deltoid cineplasties could augment existing control sources to improve control of multifunctional total arm prostheses. To explore the feasibility of these ideas, we quantified the control capabilities of individuals with preexisting biceps muscle tunnel cineplasties with the use of pursuit tracking experiments. A "proof-of-concept" EPP electric hand prosthesis was also successfully developed for a subject with agonist-antagonist, forearm tendon exteriorization cineplasties. The results of the tracking studies demonstrate numerically the efficacy of control by cineplastized muscles relative to other control approaches.

Amputation Stumps↗
PubMed1997

Excitatory amino acid receptors at a feedback pathway in the electrosensory system: implications for the searchlight hypothesis.

The electrosensory lateral line lobe (ELL) of the South American gymnotiform fish Apteronotus leptorhynchus has a laminar structure: electroreceptor afferents terminate ventrally whereas feedback input distributes to a superficial molecular layer containing the dendrites of the ELL principle (pyramidal) cells. There are two feedback pathways: a direct feedback projection that enters the ELL via a myelinated tract (stratum fibrosum, StF) and terminates in the ventral molecular layer (VML) and an indirect projection that enters as parallel fibers and terminates in the dorsal molecular layer. It has been proposed that the direct feedback pathway serves as a "searchlight" mechanism. This study characterizes StF synaptic transmission to determine whether the physiology of the direct feedback projection is consistent with this hypothesis. We used field and intracellular recordings from the ELL to investigate synaptic transmission of the StF in an in vitro slice preparation. Stimulation of the StF produced field potentials with a maximal negativity confined to a narrow band of tissue dorsal to the StF. Current source density analysis revealed two current sinks: an early sink within the StF and a later sink that corresponded to the anatomically defined VML. Field potential recordings from VML demonstrated that stimulation of the StF evoked an excitatory postsynaptic potential (EPSP) that peaked at a latency of 4-7 ms with a slow decay ( approximately 50 ms) to baseline. Intracellular recordings from pyramidal cells revealed that StF-evoked EPSPs consisted of at least two components: a fast gap junction mediated EPSP (peak 1.2-1.8 ms) and a chemical synaptic potential (peak 4-7 ms) with a slow decay phase ( approximately 50 ms). The amplitudes of the peak and decay phases of the chemical EPSP were increased by depolarizing current injection. Pharmacological studies demonstrated that the chemical EPSP was mainly due to ionotropic glutamate receptors with bothN-methyl--aspartate (NMDA) and non-NMDA components. NMDA receptors contributed substantially to both the early and late phase of the EPSP, whereas non-NMDA receptors contributed mainly to the early phase. Stimulation of the StF at physiological rates (100-200 Hz, 100 ms) produced an augmenting depolarization of the membrane potential of pyramidal cells. Temporal summation and a voltage-dependent enhancement of later EPSPs in the stimulus train permitted the compound EPSP to reach spike threshold. The nonlinear behavior of StF synaptic potentials is appropriate for the putative role of the direct feedback pathway as part of a searchlight mechanism allowing these fish to increase the electrodetectability of scanned objects.

Animals↗
PubMed1991

Oxygen transport: interrelationship between arterial pressure regulation and blood flow autoregulation.

An oxygen transport model was used to study the effects of blood flow autoregulation and arterial pressure regulation on tissue oxygen delivery. At low to moderate levels of oxygen consumption, autoregulatory increases in blood flow act in conjunction with increased tissue diffusing capacity to maintain oxygen delivery as oxygen demand becomes increased. However, an increase in the arterial pressure becomes necessary to augment oxygen delivery at higher levels of oxygen usage. At exercise levels approaching the "maximum aerobic oxygen consumption' rate, arterial pressure regulation appears to be as important as autoregulation for maintaining delivery of oxygen to the tissues. The total negative feedback gain for autoregulatory control of tissue oxygenation varies with the rate of tissue oxygen uptake and is almost 2.0 at the maximum aerobic oxygen consumption rate. Furthermore, the feedback gain is only slightly affected by changes in the mean arterial pressure that occur normally during strenuous exercise, which is indicative of the complementary relationship between these two important control mechanisms.

Biological Transport, Active↗
PubMed2002

The phosphodiesterase type 4 inhibitor, rolipram, enhances glucocorticoid receptor function.

Previous studies have demonstrated that antidepressants can enhance glucocorticoid receptor (GR) translocation and function, possibly through activation of cAMP and downstream cAMP dependent protein kinases. Accordingly, we examined GR function in cells treated with rolipram, a phosphodiesterase (PDE) type 4 inhibitor that antagonizes cAMP breakdown. Compared with vehicle-treated cells, rolipram alone and in combination with dexamethasone significantly enhanced GR function as measured in both mouse L929 cells and rat C6 glioma cells stably transfected with reporter genes driven by upstream glucocorticoid response elements. Rolipram's facilitation of GR function was reversible by the GR antagonist, RU486, and was associated with reduced cytosloic GR binding, indicating rolipram enhancement of GR nuclear translocation. Finally, rolipram potently augmented GR enhancement by the antidepressant, desipramine. These findings broaden the potential pathways by which PDE type 4 inhibitors can influence cellular function and indicate that these agents may have special utility in disorders associated with impaired GR-mediated feedback inhibition.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1995

Growth factor actions on articular cartilage.

Polypeptide growth factors play a major role in the regulation of cell behavior, including that of articular chondrocytes. Among the most influential of these factors identified for articular cartilage are insulin like growth factor I (IGF-I), basic fibroblast growth factor (bFGF), and transforming growth factor beta (TGF beta). IGF-I stimulates articular chondrocyte matrix synthetic and mitotic activity and inhibits chondrocyte mediated matrix catabolism. The role of bFGF as a potent mitogen for articular chondrocytes is well established. In contrast, this factor appears to play a complex role in matrix synthesis and degradation, promoting both anabolic and catabolic functions. Both IGF-I and bFGF have been shown to augment articular cartilage repair in vivo. TGF beta is particularly dependent upon the context in which it acts, eliciting seemingly opposite effects under different experimental conditions. These and other factors interact to modulate their respective actions, creating effector cascades and feedback loops of intercellular and intracellular events that control articular chondrocyte functions. Elucidation of the actions and interactions of these factors may be expected to clarify the etiopathogenesis of osteoarthritis and possibly offer novel methods for its treatment.

Cartilage, Articular↗
PubMed1991

Tubuloglomerular feedback in one-kidney, one-clip hypertensive rats.

Previous studies have shown that hydropenic one-kidney, one-clip (1-K, 1-C) hypertensive HT rats exhibit impaired autoregulation of glomerular filtration rate (GFR) in response to reduced arterial perfusion pressure. We investigated the possible role of altered tubuloglomerular feedback (TGF) activity in this phenomenon. Uninephrectomized Wistar rats were studied acutely 3 weeks after placing silver clips (0.2 mm) on the renal artery. Experiments were performed in 1-K,1-C HT rats and in uninephrectomized control animals. TGF activity was assessed as changes in proximal tubule stop-flow pressure (SFP) in response to orthograde microperfusion from 0 to 80 nl/min into late proximal tubule segments. Only the highest perfusion rates (approximately 40 nl/min) into late proximal tubule segments resulted in maximal decreases in SFP, indicating a marked rightward shift of overall TGF activity in 1-K,1-C HT rats. Similar responses were observed in the uninephrectomized animals. In contrast, changes of SFP were observed at lower perfusion rates in normal animals and maximal responses were observed at perfusion rates of approximately 20 nl/min. These observations are consistent with the possibility that altered TGF activity contributes to impaired autoregulation of GFR in 1-K,1-C HT rats in response to reduced renal perfusion pressure. In response to treatment with i.v. captopril, the 1-K,1-C HT rats exhibited marked decreases in systemic arterial pressure associated with decreases in SFP and virtually complete inhibition of TGF activity. It is attractive to hypothesize that these alterations in TGF characteristics in the 1-K,1-C HT rats play a significant pathophysiologic role in the acute renal dysfunction observed in response to acute decreases of blood pressure during conditions of augmented angiotensin activity. Additional future studies will allow us to address the precise role for intrarenal angiotensin in these phenomena.

Angiotensin II↗
PubMed2004

Short-term aromatase-enzyme blockade unmasks impaired feedback adaptations in luteinizing hormone and testosterone secretion in older men.

The mechanisms subserving hypoandrogenemia and relative hypogonadotropism in older men are not known. The present study tests the clinical hypothesis that aging impairs hypothalamopituitary adaptations to feedback withdrawal induced by antagonism of estrogen biosynthesis. To this end, we appraised gonadal axis responses to estrogen depletion induced by anastrozole (a potent and selective aromatase inhibitor) in nine older and 11 young men vs. placebo in 17 other older and eight young men. The study design comprised a prospectively randomized, double-blind, parallel-cohort intervention. To monitor LH release, blood was sampled every 10 min for 24 h; LH concentrations were assayed by two-site monoclonal immunoradiometric assay; pulsatile LH release quantitated by a model-free discrete peak-detection technique (Cluster); feedback-dependent orderliness of LH secretion via the approximate entropy statistic; and 24-h rhythmicity of LH concentrations by cosine analysis. At baseline, older men had comparable estradiol and testosterone but lower LH concentrations than young controls. Exposure to anastrozole reduced (24-h pooled) serum estradiol concentrations by 50% (P < 0.001) and elevated mean LH concentrations by 2.1-fold (P < 0.001) in both the young and older cohorts. However, older men failed to achieve young adult augmentation of the following: 1) total testosterone concentrations (P < 0.01) or molar testosterone to SHBG ratios (P < 0.01); 2) incremental LH pulse amplitude (P < 0.001) and LH peak area (P < 0.01); 3) mean LH pulse frequency (P = 0.0044); and 4) quantifiable irregularity (approximate entropy) of LH release patterns (P < 0.001). FSH concentrations became comparable in the two age cohorts. In summary, administration of a potent and selective aromatase antagonist reduces estradiol and elevates mean LH concentrations equivalently in young and older men. The low estrogen-feedback state in elderly men unmasks diminished incremental LH pulse amplitude and area; absence of further acceleration of LH pulse frequency; impaired regulation of the orderliness of LH release; and reduced testosterone to SHBG ratios. Thus, aging alters expected hypothalamopituitary-gonadal adaptations to short-term partial estrogen depletion in healthy men.

Adaptation, Physiological↗
PubMed2001

PKCbeta modulates antigen receptor signaling via regulation of Btk membrane localization.

Mutations in Bruton's tyrosine kinase (Btk) result in X-linked agammaglobulinemia (XLA) in humans and X-linked immunodeficiency (xid) in mice. While targeted disruption of the protein kinase C-beta (PKCbeta) gene in mice results in an immunodeficiency similar to xid, the overall tyrosine phosphorylation of Btk is significantly enhanced in PKCbeta-deficient B cells. We provide direct evidence that PKCbeta acts as a feedback loop inhibitor of Btk activation. Inhibition of PKCbeta results in a dramatic increase in B-cell receptor (BCR)-mediated Ca2+ signaling. We identified a highly conserved PKCbeta serine phosphorylation site in a short linker within the Tec homology domain of Btk. Mutation of this phosphorylation site led to enhanced tyrosine phosphorylation and membrane association of Btk, and augmented BCR and FcepsilonRI-mediated signaling in B and mast cells, respectively. These findings provide a novel mechanism whereby reversible translocation of Btk/Tec kinases regulates the threshold for immunoreceptor signaling and thereby modulates lymphocyte activation.

3T3 Cells↗
PubMed1975

Neurobiology of Stomotoca. II. Pacemakers and conduction pathways.

Evidence is presented for separate conduction pathways for swimming and for tentacle coordination in the marginal nerves of the jellyfish Stomotoca. The effector muscles are fired through junctions sensitive to excess Mg++, probably represented by the neuromuscular synapses observed by electron microscopy. The swimming effector (striated muscle) fires one-to-one with nerve input signals and myoid conduction occurs. Tentacle responses (smooth muscle contractions) involve facilitation, presumably at the neuro-effector junction; responses are graded and nonpropagating. Electrical correlates of two further conducting systems using the marginal nerves have been recorded. Their functions are unknown. One, the bridge system, extends up the four radii and encircles the peduncle; the other (ring system) is confined to the margin. A fifth conducting system is inferred in the case of the pointing response and its distribution is plotted. Signals have not been obtained from it. Pointing is accompanied by a burst of muscle potentials in the radial smooth muscles and is exhibited after a lengthy latency, indicating a local pacemaker. A sixth conducting pathway is the epithelial system, which mediates crumpling, a response involving the radial muscles without pacemaker intervention. Characteristic conduction velocities and wave forms are noted for the first four systems and for epithelial pulses. All systems, except perhaps the pointing conduction system, through-conduct under excess Mg++. Spontaneous activity patterns are described for the swimming, tentacle pulse, and ring systems. Abrupt increases in light intensity inhibit spontaneous activity, sudden decreases augmenting it. In the absence of specialized photoreceptors, light is presumed to act directly on central neurons. Epithelial pulses inhibit swimming, apparently by blocking the generation or conduction of the primary nervous events. This observation, taken in conjunction with evidence of feedback inhibition of the primary swimming system by the cells it fires, is discussed in relation to possible mechanisms whereby the output of nerve cells might be altered by activity in the excitable epithelial cells which envelop them.

Animals↗
PubMed1989

Economic correction; quantity and age-related rate of change.

Correlation between the relative magnitude of activity or concentration in youth and the relative magnitude of age-related decrease occurs in several systems. We have observed this correlation in density of D2-dopamine receptors of the striatal membrane, activity of lymphocyte activated killer cells, relative density of CD8 on thymocytes, augmenting activity of T splenocytes and mRNA, coding for IL-1 in Langerhans cells. We have suggested that this correlation should be considered in the context of balanced investment in lifespan and reproductive efficiency, that it may be the result of feedback regulation and have designated it as "economic correction".

Age Factors↗
PubMed2000

Expression and self-regulatory function of cardiac interleukin-6 during endotoxemia.

Interleukin (IL)-6 reportedly has negative inotropic and hypertrophic effects on the heart. Here, we describe endotoxin-induced IL-6 in the heart that has not previously been well characterized. An intraperitoneal injection of a bacterial lipopolysaccharide into C57BL/6 mice induced IL-6 mRNA in the heart more strongly than in any other tissue examined. Induction of mRNA for two proinflammatory cytokines, IL-1beta and tumor necrosis factor (TNF)-alpha, occurred rapidly before the induction of IL-6 mRNA and protein. Although stimulation of isolated rat neonatal myocardial cells with IL-1beta or TNF-alpha induced IL-6 mRNA in vitro, nonmyocardial heart cells produced higher levels of IL-6 mRNA upon stimulation with IL-1beta. In situ hybridization and immunohistochemical analyses localized the IL-6 expression primarily in nonmyocardial cells in vivo. Endotoxin-induced expression of cardiac IL-1beta, TNF-alpha, and intercellular adhesion molecule 1 was augmented in IL-6-deficient mice compared with control mice. Thus cardiac IL-6, expressed mainly by nonmyocardial cells via IL-1beta action during endotoxemia, is likely to suppress expression of proinflammatory mediators and to regulate itself via a negative feedback mechanism.

Animals↗
PubMed2005

Household cost-benefit equations and sustainable universal childhood immunisation: a randomised cluster controlled trial in south Pakistan [ISRCTN12421731].

BACKGROUND: Household decision-makers decide about service use based largely on the costs and perceived benefits of health interventions. Very often this leads to different decisions than those imagined by health planners, resulting in under-utilisation of public services like immunisation. In the case of Lasbela district in the south of Pakistan, only one in every ten children is immunised despite free immunisation offers by government health services. METHODS/DESIGN: In 32 communities representative of Lasbela district, 3344 households participated in a baseline survey on early child health. In the 18 randomly selected intervention communities, we will stimulate discussions on the household cost-benefit equation, as measured in the baseline. The reference (control) communities will also participate in the three annual follow-up surveys, feedback of the general survey results and the usual health promotion activities relating to immunisation, but without focussed discussion on the household cost-benefit equations. DISCUSSION: This project proposes knowledge translation as a two-way communication that can be augmented by local and international evidence. We will document cultural and contextual barriers to immunisation in the context of household cost-benefit equations. The project makes this information accessible to health managers, and reciprocally, makes information on immunisation effects and side effects available to communities. We will measure the impact of this two-way knowledge translation on immunisation uptake.

Child Health Services↗
PubMed1983

Progestin augmentation of gonadotropin-stimulated progesterone production by cultured rat granulosa cells.

Ovarian progesterone production is stimulated by FSH and LH. Concomitant treatment with a synthetic progestin, R5020, (10(-6)M) increases the FSH-stimulated production of progesterone and 20 alpha-hydroxypregn-4-en-3-one (20 alpha-OH-P) in cultured rat granulosa cells. Likewise, R5020 augments the LH-stimulated progestin production in FSH-primed cells. Furthermore, the FSH stimulation of pregnenolone biosynthesis is enhanced by 10(-6) M of progesterone or R5020. These in vitro findings suggest that progestins may exert an autoregulatory positive feedback action to enhance gonadotropin-stimulated production of progesterone and 20 alpha-OH-P.

Animals↗