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PubMed1993

Codependency: a feminist perspective.

1. Our understanding of psychological life has been underdeveloped and distorted because explanations have been created by only one half of the human species. The current broad and encompassing disease definition of codependency may devalue some of women's greatest strengths. 2. The disease model of codependency, it may be argued, is rooted in extant, reductionist models that suggest a developmental pathway of separation and individuation leading to an autonomous and independent maturity. 3. The feminist model of Growth in Connection proposes that the flowering of the self occurs within the development and maintenance of relationships in which accurate and mutual empathy is both the goal and the motivation toward growth.

Codependency, Psychological↗
PubMed2001

How the brain regulates food intake and body weight: the role of leptin.

The brain plays a key role in the regulation of energy homeostasis, balancing food intake and energy expenditure to maintain adipose tissue mass. A widely accepted model proposes that energy homeostasis is modulated by hormones that circulate in the blood in proportion to adipose tissue mass. A major candidate 'adiposity signal' to the brain is the adipocyte hormone, leptin; this inhibits neuropeptide circuits that promote anabolic metabolism, and stimulates those that promote catabolic metabolism. It is hypothesized that leptin-responsive circuits in the hypothalamus project to caudal brainstem neuronal groups that integrate satiety signals converging on the brain from the stomach and intestine following ingestion of food. Leptin signaling to the brainstem via hypothalamic pathways potentially increases the brain's motor and autonomic responses to satiety signals, leading to smaller individual meals, reduced cumulative food intake, and a lower body weight. This mechanism explains how leptin deficiency or defects in the brain's processing of leptin signaling can result in a sustained increase in food intake and obesity.

Adipose Tissue↗
PubMed1975

Tryptophan metabolism in skin diseases.

In a number of skin disturbances conditioned or aggravated by sunlight and/or mainly diffused to the cutaneous connective tissue (present acquired pellagra, lupus erythematosus, porphyria cutanea tarda, actinic reticuloid, Rothmund-Thomson syndrome, lymphocytoma cutis, scleroderma, dermatomyositis, burns, linphomas, parapsoriasis, acrodermatitis enteropathica) excretive changes were found only in the "via kynurenine" metabolites. As a rule kynureniase activity was reduced and tryptophan-pyrrolase activity was increased. In the epidermis tryptophan leads to niacin pathway was found to be present and sometimes autonomous.

Animals↗
PubMed1992

Human 55-kDa receptor for tumor necrosis factor coupled to signal transduction cascades.

The numerous biological activities of tumor necrosis factor (TNF) appear mediated by two types of receptors of 55 kDa (TR55) and 75 kDa (TR75) molecular mass. To test TR55 for its individual role in signaling across the membrane, a cDNA coding for the human TR55 was stably expressed in murine 70Z/3 pre-B cells, which lack binding sites for, and proved nonresponsive to human TNF. The transfected TR55 showed high affinity ligand binding and active internalization. It is demonstrated that the TNF signaling cascade, i.e. stimulation of protein kinase C, sphingomyelinase, and phospholipase A2, production of the second messengers diacylglycerol and ceramide, can occur completely through exclusive binding of TNF to TR55. The p55 TNF-binding site functions as an autonomous TNF receptor that mediates key signal transduction pathways, which may control the majority of TNF actions.

Animals↗
PubMed2000

IUPHAR Southeast Asian-Western Pacific Region--eighth Meeting. Pharmacology in the Next Millennium. 1-5 November 1999, Taipei, Taiwan.

This conference focused on some areas of particular interest to pharmacologists in the Asia-Pacific region, including prostanoids, drug metabolism and drugs from traditional Chinese herbs. Areas covered in the prostanoid sessions included reviews of the development of selective COX-2 inhibitors, the use of knockout mice to study the role of prostanoid receptors in various disease states, the interactions of G-protein-coupled receptor pathways, and the effects of prostanoid mimetics on autonomic neurons. Sessions on drug metabolism reviewed the use of transgenic mouse models for toxicological screening of new drugs, the use of a combination of probe drugs given together to identify the activity of a range of drug metabolizing enzymes in vivo, and the interaction of drug metabolizing enzymes and nitric oxide. In the presentations on herbal medicines, there were discussions about the regulatory status and the problems involved in conducting clinical trials with these preparations. There were a number of seminars on details of the basic or clinical pharmacology of some active principles derived from herbs, thus recognizing the intense effort by local pharmacologists to improve the scientific study of this important resource.

Journal Article↗
PubMed1985

Sympathetic nervous adjustments in man to simulated weightlessness induced by water immersion.

To clarify the role of the sympathetic nervous system to adjust the fluid shift under weightlessness, muscle and skin sympathetic activities were recorded microneurographically in human subjects under simulated weightlessness induced by water immersion up to the levels of the knee, the navel, the breast and the neck. The muscle and skin sympathetic activities were reduced in proportion to rise of immersion level up to the neck. These changes of sympathetic activities were almost concomitant with those of simultaneously recorded soleus electromyograms and heart rate. Reductions of the thigh and the leg circumference were also confirmed by strain gauge plethysmogram recorded under the same experimental condition. Based on these findings, it is concluded that the sympathetic nervous system is suppressed under weightlessness simulated by water immersion. This suppression might depend mainly on the activation of intrathoracic low pressure receptors, due to the fluid shift toward the upper part of the body. The suppression of the sympathetic nervous system seems to be important to compensate the fluid shift under weightlessness.

Adult↗
PubMed1975

[Hypothalamus: some diagnostic principles].

The hypothalamus is a small group of receptors for visceral control, receiving influences from other parts of the nervous system. In turn, some hypothalamic nuclei send efferent impulses to the neurohypophysis, back along limbic pathways to the cortex and down to the autonomic centers in the brain stem. Not all the experimental observations on lower vertebrates can be applied to hypothalamic nuclear areas and connections in man. Therefore, knowledge of such functions and clinical syndromes as those relating to regulation of cardiovascular system, temperature, feeding, drinking, electrolyte balance and the sleeping-waking cycle continues to be incomplete.

Brain Diseases↗
PubMed1995

Effects of arginine-lysine mixture, glucose and ATP on the autonomic outflows to the thymus and spleen.

Effect of arginine-lysine mixture, glucose and ATP on the efferent activities of the vagal thymic branch and splenic nerve were studied in urethane anesthetized rat. In male Wistar rats jugular vein was cannulated for drug administration. In one group the thymus was exposed and a nerve filament of the central cut end of vagal thymus was isolated. In another group a filament was isolated from that of the splenic nerve. The nerve filament was placed on electrodes to record efferent activity before and after administration of argininelysine mixture solution, glucose or ATP solution. Enhancement of efferent activity of vagal thymic nerve was observed after i.v. administration of arginine-lysine mixture, glucose and ATP solution. Suppression in efferent activity of splenic nerve was investigated following i.v. administration of arginine-lysine mixture, glucose and ATP solution. These results suggest that i.v. arginine-lysine, glucose and ATP increase thymic lymphocyte release, and that i.v. arginine-lysine, glucose and ATP enhance NK cell activity.

Adenosine Monophosphate↗
PubMed1995

Study on vomiting related to the vestibulo-autonomic reflex.

The purpose of this study was to investigate the neural pathway from the vestibular labyrinth to the medullary vomiting center in the cat, using electrophysiological techniques. During electrical stimulation of the canal nerve, we found conflicting results: the pressure in the stomach sometimes increased, and sometimes decreased. There might be several neural structures between the semicircular canal nerve and the vomiting center in the dorsolateral portion of the reticular formation of medulla oblongata. Retching or vomiting-like behavior during both respiration and movement of the stomach was recorded during stimulation at several sites in the lateral medullary reticular formation. However, the evoked unit activities were not always induced by stimulation of the canal nerve.

Animals↗
PubMed2005

Beta2-agonist and anticholinergic drugs in the treatment of lung disease.

The lungs are innervated by both the sympathetic and parasympathetic nervous systems, which entails the activation of adrenergic and muscarinic receptors, respectively. Both the adrenergic and muscarinic receptors are G-protein-coupled receptors, and they share many similar signal transduction molecules. These receptors are widely expressed in the lung and the specific receptor expression can vary among the species. The location and the subtype of receptor expressed are important in the regulation of normal airway function. Acetylcholine released from the parasympathetic fibers activates the M3 muscarinic receptors located on the airway smooth muscle, causing bronchoconstriction. To counter this activity, M2 muscarinic receptors located on the parasympathetic nerves inhibit release of acetylcholine. Beta2-adrenergic receptors are expressed on the airway smooth muscle where activation causes bronchodilation. Adrenergic receptors are also on the autonomic nerves where they can modulate neurotransmitter release. The crosstalk between these G-protein-coupled receptors and downstream pathways ensures normal airway function. The prejunctional and postjunctional muscarinic and adrenergic receptors control autonomic tone and any imbalance or selective blockade of the receptors can compromise the system and cause the airways to become hyperreactive. The location, function, and crosstalk of the adrenergic and muscarinic receptors must be considered in the design, development, and use of drugs to combat airway diseases.

Adrenergic beta-Agonists↗
PubMed2001

Transmission in autonomic ganglia.

The activity of airway smooth muscle, glands and vasculature is under tonic control by the autonomic nervous system. Information regarding the function and state of the airway (e.g. blood flow, temperature, oxygen levels, movement, irritants, inflammation, etc.) is relayed to the central nervous system (CNS) in the form of action potentials carried by sensory nerves. This input is integrated at many levels in the CNS and this information is ultimately transformed into coded action potentials carried by various preganglionic nerve pathways from the CNS to peripheral clusters of neurons referred to as autonomic ganglia. In the autonomic ganglia the CNS-derived action potentials cause the release of neurotransmitter(s) at a synapse between the preganglionic nerve terminal and the principal ganglion neuron. The fact that synaptic transmission exists makes the ganglion neuron the final site of integration in this complex reflex pathway. Whether this transmission of information from the CNS occurs, by activating the autonomic ganglion neuron and consequently the effector organ, depends on neurochemical, anatomical, and electrophysiological factors within the ganglion that is the subject of this review.

Animals↗
PubMedDate not supplied

Evaluation of the vagal-sympathetic interaction in diabetics with autonomic neuropathy through power spectrum density analysis of the heart rate. A critical revision of the natural history of diabetic autonomic neuropathy is possible.

In this paper we apply spectral analysis methods to heart rate variability to assess the autonomic nervous system activity in normal subjects and in patients affected by different degrees of diabetic autonomic neuropathy. The current opinion, based on different clinical tests, is that parasympathetic impairment occurs earlier in autonomic dysfunctions. However, the use of power spectrum density analysis based on a single parameter (heart rate) suggests a simultaneous involvement of parasympathetic and sympathetic pathways leading to the conclusion that perhaps the natural history of diabetic autonomic neuropathy should be substantially rewritten.

Autonomic Nervous System Diseases↗
PubMed2005

Primary neurologic screening and motor coordination of Dstdt-J mutant mice (dystonia musculorum) with spinocerebellar atrophy.

The autosomal recessive dystonia musculorum (Dst(dt-J)) mutation causes degenerative lesions of peripheral and central sensory pathways. A test battery of motor, sensory, postural, and autonomic functions was used to compare young control and homozygous Dst(dt-J) mice. The Dst(dt-J) mutants were severely impaired for muscle strength, limb coordination, and postural reflexes. As a result of a loss in motor control, the mutants were hypoactive in the open-field and fell quickly from the stationary beam. In sensory tests, the acoustic startle response was impaired, but not tactile reflexes and contact righting, attesting to preserved labyrinthine function and non-lemniscal pathways. Dst(dt-J) mutants were also distinguishable from controls on the basis of tremor, a paler skin, piloerection, and half-open eyes, as well as low body weight and fecal boli. Grooming episodes were less frequent in the mutants but without any reduction in grooming time. The neurologic screening battery delineated the functional integrity of some sensorimotor pathways in a spinocerebellar mutant whose severe phenotype prevents a more elaborate evaluation.

Analysis of Variance↗
PubMedDate not supplied

Interactions between autonomic nervous system activity and endothelial function: a model for the development of cardiovascular disease.

OBJECTIVES: Endothelial dysfunction is a new pathway in cardiovascular disease (CVD) development. Psychosocial factors have been little studied in relation to endothelial function, although they may interact via associations with the autonomic nervous system (ANS). The purpose of this review is to propose a model by which psychosocial factors are related to CVD development through interactions between the ANS and vascular endothelium. METHODS: The literature supporting an interaction between the ANS and endothelium in healthy and disease states is reviewed. Potential mechanisms linking the two systems are explored as a pathway for CVD development. RESULTS: Endothelial dysfunction and impaired cardiovascular ANS regulation are both markers for increased CVD risk. Sympathetic nerves and vascular endothelial cells share a functional antagonism in healthy states to maintain appropriate blood vessel tone. Alterations in sympathetic activity and endothelial cell function are both observed early in the development of CVD and may result from an inability to maintain the functional antagonism. Impairments in either ANS regulation or endothelial function may contribute to further disease development by evoking maladaptive changes in the opposing system. CONCLUSIONS: Although interactions between cardiovascular ANS regulation and endothelial function are likely involved in CVD development, further research is needed to determine whether ANS and endothelium interactions are a plausible pathway linking psychosocial factors with increased CVD risk.

Adult↗
PubMed2003

Central nuclei mediating estrogen-induced changes in autonomic tone and baroreceptor reflex in male rats.

The current investigation examines the significance of estrogen in central cardiovascular regulatory nuclei in modulating autonomic tone and baroreceptor reflex function. Experiments were done in anaesthetized male Sprague-Dawley rats. Changes in autonomic tone were assessed by monitoring vagal and renal efferent nerve activities before and following bilateral injection of estrogen into select central autonomic nuclei. In the first study, selective blockade of neurotransmission through the central nucleus of the amygdala (CNA), lateral hypothalamic area (LHA) and ventral posteromedial thalamic nucleus (VPM) using the local anaesthetic lidocaine was done to determine which nuclei were involved in mediating the autonomic changes observed following bilateral injections of estrogen into the insular cortex (IC). In the second study, the role of the parabrachial nucleus (PBN) in mediating the autonomic changes observed following bilateral estrogen injections into the CNA, LHA, VPM and IC was determined by blocking neurotransmission through the PBN using lidocaine.Injections of estrogen into the IC produced a significant increase in renal sympathetic nerve activity (RSNA; from 10+/-2 to 24+/-4 microV/sec; p<0.05). This estrogen-induced increase in RSNA was significantly attenuated when lidocaine was pre-injected into the LHA, CNA or PBN (55+/-6, 33+/-4 and 91+/-7% decrease respectively; p<0.05) but not when injected into the VPM (16+/-6% decrease; p>0.05). Injection of estrogen into the CNA resulted in a significant decrease in RSNA (48+/-5%; p<0.05) whereas estrogen injection into the LHA resulted in a significant increase (28+/-4%; p<0.05) in RSNA. Pre-injection of lidocaine into the PBN resulted in complete blockade of the autonomic changes observed following estrogen injection into the CNA but did not affect the changes observed following estrogen injection into the LHA. These results suggest that estrogen acting in forebrain and midbrain cardiovascular nuclei activated efferent pathways which synapse in the LHA, CNA and/or PBN prior to projecting to autonomic preganglionic nuclei to affect autonomic tone. These nuclei may therefore provide an added level of processing and/or integration of the autonomic response(s) following activation by local or systemic estrogen.

Amygdala↗