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At least 487 records · Page 27Linked to original sources
PubMed1997

Anatomy of schizophrenia revisited.

The search for an anatomy of schizophrenia has engendered an enormous, almost indigestible mass of data. In no studies do all patients show the same deviations from control samples. No morphological or microscopic abnormality has been found that is either necessary or sufficient for the diagnosis. In contrast to epilepsy, in which a proliferation of excitatory pathways or inadequate inhibitory factors are paramount, schizophrenia may represent a genetically and age-determined elaboration of one or more inhibitory networks in response to specific physiological events (e.g., the increased neuronal activity in limbic and hypothalamic structures during the physiological events of puberty) or to brain injury or defect. Current diagnostic classifications, including the positive-negative categories, have not led to separation of the disorder into etiologically or pathologically similar subgroups. Analysis of morphological and other biological pathology by a different nosological principle, such as trajectory of the illness, and separate correlation of anatomical and other biological outliers with clinical and demographic factors may be more successful strategies than pooling and averaging results from a mixture of patients diagnosed with schizophrenia.

Brain↗
PubMed2006

Psychological job demands increase the risk of ischaemic heart disease: a 14-year cohort study of employed Danish men.

AIMS: To test the relationship between job strain and the incidence of ischaemic heart disease (IHD) prospectively in the Danish working population. METHODS AND RESULTS: In 1986, a clinical examination was undertaken of 659 men, all employed and without known IHD, together with a questionnaire-based evaluation of living conditions and psychosocial factors at work, including items identified in the job strain model. This study was part of the World Health Organization-initiated MONICA II study. In the job strain model, job strain is defined as the combination of high psychological demands and a low degree of control in the work situation. An objective classification of the components in the job strain model was made by imputation by utilizing the participants' job title and the principles guiding the payment of their salaries/wages. In addition, a questionnaire-based subjective classification was undertaken. All participants were followed until the end of 1999 with regard to hospitalization and death as a result of IHD. Stepwise analyses were made, adjusting for age, social class, social network and established behavioural and physiological coronary risk factors. Self-reported job strain was significantly associated with IHD independently of standard coronary risk factors. Of the two components in the job strain model only high demands contributed significantly to this result. The study did not support the job strain hypothesis when an imputed, objective classification of the components in the job strain model was applied. This is in accordance with the majority of other studies in this area. An unexpected finding was that the incidence of IHD was highest among employers and managers. CONCLUSION: High psychological demands at work are a risk factor for IHD, a fact that should affect the primary and secondary prevention of IHD.

Adult↗
PubMed2003

Interindividual variations in constitutive interleukin-10 messenger RNA and protein levels and their association with genetic polymorphisms.

BACKGROUND: Genetic variations in the interleukin (IL)-10 gene promoter have been associated with levels of induced production of IL-10, disease susceptibility, and allograft rejection. Small amounts of this cytokine are constitutively produced and are important in maintaining the physiologic function of the cytokine network. In this study, we evaluated the distribution of IL-10 basal levels and its genetic regulation in a healthy Spanish population. METHODS: Polymorphisms at the -1,082, -819, and -512 positions of the IL-10 promoter were analyzed by polymerase chain reaction amplification and hybridization with fluorescent-labeled allele-specific probes in 183 Spanish people. Levels of IL-10 messenger (m)RNA were tested by real-time reverse transcription-polymerase chain reaction in 123 healthy donors. Serum concentrations of IL-10 were measured by a highly sensitive ELISA, whereas protein amounts in lipopolysaccharide culture supernatants were quantified by an in-house ELISA. RESULTS: The frequency of IL-10 promoter alleles and haplotypes in our population showed remarkable differences from other Caucasian populations. Large interindividual variations were found in mRNA and protein constitutive levels of IL-10, which allowed its classification in low and intermediate/high producers. We found statistical differences in mRNA concentration between the polymorphic variant GCC/GCC and the low producer genotypes. The G allele at position -1082 was the most important genetic factor in the regulation of constitutive IL-10 mRNA levels. Similarly, we also found an association of this polymorphic position with serum concentration greater than 2 pg/mL. CONCLUSIONS: Constitutive levels of IL-10 (mRNA and serum protein) displayed remarkable interindividual variations, which are genetically controlled by polymorphic variants at the cytokine gene promoter.

Alleles↗
PubMedDate not supplied

Hippocampal CA3 region predicts memory sequences: accounting for the phase precession of place cells.

Hippocampal recordings show that different place cells fire at different phases during the same theta oscillation, probably at the peak of different gamma cycles. As the rat moves through the place field of a given cell, the phase of firing during the theta cycle advances progressively. In this paper we have sought to determine whether a recently developed model of hippocampal and cortical memory function can explain this phase advance and other properties of place cells. According to this physiologically based model, the CA3 network stores information about the sequence of places traversed during learning. Here we show that the phase advance can be understood if it is assumed that the hippocampus is in a recall mode that operates when the animal is already familiar with a path. In this mode, sensory information about the current position triggers recall of the upcoming 5-6 places (memories) in the path at a rate of one memory per gamma cycle. The model predicts that the average phase advance will be one gamma cycle per theta cycle, a value in reasonable agreement with the data. The model also correctly accounts for (1) the fact that the firing of a place cell occurs during approximately 7 theta cycles (on average) as the animal crosses the place field; (2) the observation that the phase of place cell firing depends more systematically on position than on time; and (3) the fact that traversal of an already familiar path produces further modifications (shifts the firing of a cell to an earlier position in the path). This later finding suggests that recall of previously stored information strengthens the memory of that information. In the model, this occurs because of a novel role of N-methyl-D-aspartate channels in recall. The general success of the model provides support for the idea that the hippocampus stores sequence information and makes predictions of expected positions during gamma-frequency recall.

Computer Simulation↗
PubMed2002

Carbon catabolite repression in bacteria: choice of the carbon source and autoregulatory limitation of sugar utilization.

Carbon catabolite repression (CCR) in bacteria is generally regarded as a regulatory mechanism to ensure sequential utilization of carbohydrates. Selection of the carbon sources is mainly made at the level of carbohydrate-specific induction. Since virtually all carbohydrate catabolic genes or operons are regulated by specific control proteins and require inducers for high level expression, direct control of the activity of regulators or control of inducer formation is an efficient measure to keep them silent. By these mechanisms, bacteria are able to establish a hierarchy of sugar utilization. In addition to the control of induction processes by CCR, bacteria have developed global transcriptional regulation circuits, in which pleiotropic regulators are activated. These global control proteins, the catabolite gene activator protein (CAP), also known as cAMP receptor protein, in Escherichia coli or the catabolite control protein (CcpA) in Gram-positive bacteria with low GC content, act upon a large number of catabolic genes/operons. Since practically any carbon source is able to trigger global transcriptional control, expression of sugar utilization genes is restricted even in the sole presence of their cognate substrates. Consequently, CAP- or CcpA-dependent catabolite repression serves as an autoregulatory device to keep sugar utilization at a certain level rather than to establish preferential utilization of certain carbon sources. Together with other autoregulatory mechanisms that are not acting at the gene expression level, CCR helps bacteria to adjust sugar utilization to their metabolic capacities. Therefore, catabolic/metabolic balance would perhaps better describe the physiological role of this regulatory network than the term catabolite repression.

Bacteria↗
PubMed1993

Demonstration of pulmonary vascular perfusion by electron and light microscopy.

To estimate the fraction of dense pulmonary capillary network that is perfused under physiological conditions, we developed a new method for the demonstration of in vivo capillary perfusion by light and electron microscopy. Blood plasma was labeled by 8-nm colloidal gold particles coated with rabbit serum albumin. In anesthetized rabbits, 4-5 ml of this tracer were injected into the right atrium. Two and 15 min later, the circulation was interrupted by a snare around the heart, and the lung was fixed by instillation with glutaraldehyde. Gold particles were found in the plasma space of alveolar capillaries as well as in other organs. A random sample of thin sections studied by electron microscopy revealed that the entire capillary bed of the lung was perfused at least with plasma within 2 min after tracer infusion. Light microscopy of silver-enhanced sections showed areas with different staining intensities but no obviously unperfused capillaries. The concept of capillary recruitment, which would require a significant fraction of capillaries unperfused at rest, may have to be reassessed to consider time factors as well as the two-phase nature of blood; red blood cells and plasma may take different paths.

Animals↗
PubMed2003

Interactions between membrane conductances underlying thalamocortical slow-wave oscillations.

Neurons of the central nervous system display a broad spectrum of intrinsic electrophysiological properties that are absent in the traditional "integrate-and-fire" model. A network of neurons with these properties interacting through synaptic receptors with many time scales can produce complex patterns of activity that cannot be intuitively predicted. Computational methods, tightly linked to experimental data, provide insights into the dynamics of neural networks. We review this approach for the case of bursting neurons of the thalamus, with a focus on thalamic and thalamocortical slow-wave oscillations. At the single-cell level, intrinsic bursting or oscillations can be explained by interactions between calcium- and voltage-dependent channels. At the network level, the genesis of oscillations, their initiation, propagation, termination, and large-scale synchrony can be explained by interactions between neurons with a variety of intrinsic cellular properties through different types of synaptic receptors. These interactions can be altered by neuromodulators, which can dramatically shift the large-scale behavior of the network, and can also be disrupted in many ways, resulting in pathological patterns of activity, such as seizures. We suggest a coherent framework that accounts for a large body of experimental data at the ion-channel, single-cell, and network levels. This framework suggests physiological roles for the highly synchronized oscillations of slow-wave sleep.

Action Potentials↗
PubMed1995

How precise is neuronal synchronization?

Recent work suggests that synchronization of neuronal activity could serve to define functionally relevant relationships between spatially distributed cortical neurons. At present, it is not known to what extent this hypothesis is compatible with the widely supported notion of coarse coding, which assumes that features of a stimulus are represented by the graded responses of a population of optimally and suboptimally activated cells. To resolve this issue we investigated the temporal relationship between responses of optimally and suboptimally stimulated neurons in area 17 of cat visual cortex. We find that optimally and suboptimally activated cells can synchronize their responses with a precision of a few milliseconds. However, there are consistent and systematic deviations of the phase relations from zero phase lag. Systematic variation of the orientation of visual stimuli shows that optimally driven neurons tend to lead over suboptimally activated cells. The observed phase lag depends linearly on the stimulus orientation and is, in addition, proportional to the difference between the preferred orientations of the recorded cells. Similar effects occur when testing the influence of the movement direction and the spatial frequency of visual stimuli. These results suggest that binding by synchrony can be used to define assemblies of neurons representing a coarse-coded stimulus. Furthermore, they allow a quantitative test of neuronal network models designed to reproduce physiological results on stimulus-specific synchronization.

Anesthesia↗
PubMed2006

Dynamic interactions between myocytes, fibroblasts, and extracellular matrix.

Cardiac function is determined by the coordinated and dynamic interaction of several cell types together with components of the extracellular matrix (ECM). This interaction is regulated by mechanical, chemical, and electrical signals between the cellular and noncellular components of the heart. Recent studies using fluorescence-activated cell sorting indicate that the number of myocytes remains relatively constant during development and disease, whereas the number of fibroblasts and other cell types can change dramatically. Cardiac fibroblasts appear to have different origins at different stages of development and fluctuate in response to a variety of physiological signals. Fibroblasts form a network of cells that are connected to each other via specific cadherins and connexins, to the ECM via integrins, and to myocytes by a variety of receptors, including connexins. Examples of the integration of signals include the role of angiotensin II (Ang II), which stimulates mechanical contraction of fibroblasts, as well as cytokine signaling. Cytokine signaling alters connexin and K(+) channel activation, which in turn is regulated by Ang II, essentially forming a feedback loop. Quantitative changes in mechanical, chemical, and electrical signals that can alter the overall cardiac form and function will be discussed here.

Animals↗
PubMed1992

Evidence for a negative ultrashort loop feedback regulating galanin release from the arcuate nucleus-median eminence functional unit.

Recent studies from our laboratory have demonstrated that galanin (GAL) is a member of the hypothalamic-hypophysiotropic hormone family. Most of the hypothalamic hormones regulate their own secretion rate by ultrashort loop feedback mechanisms. The purpose of these studies was to evaluate the possibility that hypothalamic GAL could regulate its own release through a similar mechanism. Galanin secretion from median eminence (ME) fragments incubated in vitro increased exponentially with time, whereas GAL release from arcuate nucleus-ME (AN-ME) fragments depicted a secretory profile consisting of an initial exponential rising phase, followed by a plateau phase in which GAL secretion was apparently abolished. Moreover, preexposure of AN-ME fragments to porcine GAL (pGAL) increased tissue responsiveness to K(+)-induced depolarization, suggesting that pGAL reduced the gain of the system. Thus, after pGAL removal, AN-ME fragments appear to be more sensitive to the depolarizing stimulus. In addition, blockade of GAL biological activity in vivo by administration of a sheep antirat GAL serum increased GAL release from AN-ME fragments in vitro, whereas this treatment did not affect GAL release from ME terminals. These results indicate that GAL neurons may diminish their own activity, establishing, therefore, a negative ultrashort loop feedback that controls the firing of the AN galaninergic network and maintains a balanced physiological status. By means of electron microscopy, we demonstrated that GAL-containing perikarya and proximal dendrites receive synapsing axons immunoreactive for the same peptide in the AN, which provides the anatomical basis for interactions between galaninergic neurons. In conclusion, our data support the notion that the galaninergic system, as other peptidergic neurotransmitters, is able to regulate its own release via a negative ultrashort loop feedback control mechanism that is operative at the level of the AN.

Animals↗
PubMed1997

Pulsating fluid flow stimulates prostaglandin release and inducible prostaglandin G/H synthase mRNA expression in primary mouse bone cells.

Bone tissue responds to mechanical stress with adaptive changes in mass and structure. Mechanical stress produces flow of fluid in the osteocyte lacunar-canalicular network, which is likely the physiological signal for bone cell adaptive responses. We examined the effects of 1 h pulsating fluid flow (PFF; 0.7 +/- 0.02 Pa, 5 Hz) on prostaglandin (PG) E2, PGI2, and PGF2alpha production and on the expression of the constitutive and inducible prostaglandin G/H synthases, PGHS-1, and PGHS-2, the major enzymes in the conversion of arachidonic acid to prostaglandins, using mouse calvarial bone cell cultures. PFF treatment stimulated the release of all three prostaglandins under 2% serum conditions, but with a different time course and to a different extent. PGF2alpha was rapidly increased 5-10 minutes after the onset of PFF. PGE2 release increased somewhat more slowly (significant after 10 minutes), but continued throughout 60 minutes of treatment. The response of PGI2 was the slowest, and only significant after 30 and 60 minutes of treatment. In addition, PFF induced the expression of PGHS-2 but not PGHS-1. One hour of PFF treatment increased PGHS-2 mRNA expression about 2-fold relative to the induction by 2% fresh serum given at the start of PFF. When the addition of fresh serum was reduced to 0.1%, the induction of PGHS-2 was 8- to 9-fold in PFF-treated cells relative to controls. This up-regulation continued for at least 1 h after PFF removal. PFF also markedly increased PGHS activity, measured as the conversion of arachidonic acid into PGE2. One hour after PFF removal, the production of all three prostaglandins was still enhanced. These results suggest that prostaglandins are important early mediators of the response of bone cells to mechanical stress. Prostaglandin up-regulation is associated with an induction of PGHS-2 enzyme mRNA, which may subsequently provide a means for amplifying the cellular response to mechanical stress.

Analysis of Variance↗
PubMed1988

Modulation of thymic endocrine function by thyroid and steroid hormones.

The thymic epithelium is responsible for the secretion of thymic hormones that intervene in some steps of intra- and extra-thymic T cell differentiation. In the present paper, we studied the in vivo and in vitro influences of thyroid and steroid hormones on the secretion of thymulin, one of the chemically-defined thymic hormones. Triodothyronine injected in young mice or applied into supernatants of cultured thymic epithelial cells resulted in an increase of thymulin synthesis and secretion, respectively evaluated by the analyses of thymulin containing cells and thymulin levels. The influence of steroids was investigated in vivo by steroid depletion (adrenalectomy and/or castration) and in vitro by the addition of various steroids and/or their specific antagonists to cultured thymic epithelial cells. Surgical ablation of adrenals and/or gonads induced a transient depletion of circulating thymulin and, by feedback mechanism, an increase in the numbers of thymulin containing cells. From the in vitro data we could conclude that the various steroid hormones (that exhibited a stimulatory effect) can act directly on the thymic epithelium, probably via specific receptors. The bulk of data above described represents a strong evidence for the physiological involvement of the neuroendocrine network, on the hormonal function of the thymic epithelium.

Adrenal Cortex Hormones↗
PubMed2005

Functional eicosanoid test and typing (FET) of peripheral blood cells in eicosanoids related diseases.

Monitoring of eicosanoid synthesis in peripheral blood cells has significant potential for improving the diagnosis and therapy of many human diseases. The quantitative relation between concentrations of prostaglandins and leukotrienes is central to the physiologic function of the eicosanoid network. Here we show that this regulation, which we call the functional eicosanoid typing (FET), fluctuates dynamically in individual living blood cells from patients, thereby limiting the accuracy with which concentration circuits of eicosanoids can transfer metabolic information. Using living cells in functional cell testing, we characterised the eicosanoid pattern score (EPS). A novel technique based on binomial errors on lipid mediator partitioning enabled calibration of in vivo biochemical parameters in molecular units. We found that eicosanoid production rates fluctuate over a time scale of about twenty minutes, while intrinsic noise decays rapidly. Thus, biochemical eicosanoid parameters, noise, and slowly varying cellular states together determine the effective FET. These results can form a basis for quantitative modelling of natural eicosanoid circuits in diagnosis of eicosanoid related diseases and design of synthetic ones for the prediction other diseases.

Adult↗
PubMed1991

Cytokine expression in T-cell lymphomas and Hodgkin's disease. Its possible implication in autocrine or paracrine production as a potential basis for neoplastic growth.

The detection of an increasing number of cytokines and the demonstration of autocrine and paracrine mechanisms perpetuating tumor growth prompted the investigation of the expression of the cytokines IL-2, IL-3, IL-4, IL-5, IL-6, IFN gamma, Tac, and GMCSF in primary lymph-node biopsies of patients with peripheral T-cell lymphoma (n = 11), Hodgkin's disease (n = 13), and large-cell anaplastic lymphoma (n = 6) by means of Northern blot analysis and in situ hybridization (ISH); 15 of 28 cases had IL-6 message, predominantly in cases of Hodgkin's disease (HD) and large-cell anaplastic lymphomas (LCAL). Interferon gamma was found in about 50% of the cases among all entities. Other cytokine expression was rare except two cases of HD with high amounts of IL-4 mRNA. These results indicate that large amounts of growth factor transcripts are present in a variety of malignant lymphomas. The meaning of this expression is still unclear. It may be a loss of physiologic regulation within the cytokine network which may thus influence neoplastic cell growth as some cases have a quantity of cytokine expression which is similar or even above that of stimulated T cells. ISH demonstrates in individual cases that the expression is at least in part due to malignant cells.

Antibodies, Monoclonal↗
PubMed1989

Concepts in immunodermatology.

This review describes the various processes which take place in the immunological network of the skin under physiologic or pathological circumstances. A full understanding of the mechanisms in action is important as it could lead to the development of an entirely new class of therapeutics.

Antigen-Presenting Cells↗
PubMedDate not supplied

[Microsurgical anatomy of extraorganic arteries of the hypothalamo-hypophyseal complex and the rational technic of its removal for transplantation].

The authors ascertained the existence of numerous anastomoses between the right and left hypophyseal arteries on the level of both the interlobar sulcus and the base of the hypophyseal funnel in the form of an inferior and superior hypophyseal anastomotic rings, as well as a system of arterial connections between the anterosuperior and anteroinferior subgroups of the hypothalamic arteries located in front of and lateral to the chiasma as prechiasmal networks. This creates anatomo-physiological preconditions for adequate circulation in the hypothalamo-hypophyseal graft after its transplantation and inclusion in the blood flow of the internal carotid artery or one of its terminal branches. Bearing in mind the close connection of the hypophyseal and hypothalamic arteries with the cavernous sinuses, chiasma, and components of the sella turcica, the hypothalamo-hypophyseal graft must be removed in a complex with these structures.

Anthropometry↗
PubMed1986

Diabetic papillopathy: fluorangiographic aspects.

Diabetic papillopathy is one of the signs of diabetic microangiopathy. Up to now several researchers have taken interest in this disease, providing various and sometimes clashing pathogenetical interpretations. The most plausible gives a major importance to a localized damage of the peripapillary vascular radial network, considering the anatomo-physiological features of this structure. The Authors' survey is presented with particular attention to fluorangiographic aspects of papillary changes.

Adult↗
PubMed1983

Effect of prostacyclin (PGI2) on immune-complex-induced neutropenia.

This study reports the results of in vitro and in vivo investigations on the effect of prostacyclin (PGI2) on polymorphonuclear neutrophils (PMN) challenged with immune complexes (IC). In vitro, PGI2 does not affect the interaction of IC with PMN membrane receptors, but prevents the ensuing PMN aggregation and secretion of platelet-activating factor, a lipid mediator responsible for immune-induced PMN aggregation. In vivo, the infusion of PGI2 in New Zealand white rabbits injected with IC prevents IC-induced neutropenia and thrombocytopenia as well as the embolization of PMN into the pulmonary peripheral capillary network. These results suggest a physiological role for PGI2 in modulating the interaction between IC and PMN.

Agranulocytosis↗