Neurobiology of Pain in Children: An Overview

The evaluation of pain in the newborn and the infant is difficult because pain is mainly a subjective phenomenon. Until a few years ago, several myths persisted. First, the myth that children, especially infants, do not feel pain the way adults do, therefore there is no untoward consequences for them. Second, lack of assessment and reassessment for the presence of pain. Third, misunderstanding of how to conceptualise and quantify a subjective experience. Fourth, lack of knowledge of pain treatment. Fifth, the notion that addressing pain in children takes too much time and effort, in ultimate analysis resulting in wasting time. Sixth, fears of hidden -and not easy to diagnose or prevent- adverse effects of analgesic medications, including respiratory depression and addiction. Finally, from a conceptual point of view, high thresholds of pain in neonates and infants were considered to be present by natural character, and useful in protecting infant from pain during birth and transit through the narrow vaginal channel

Potential Therapeutic Effects of Vitamin E and C on Placental Oxidative Stress Induced by Nicotine: An In Vitro Evidence

There have been a few studies that examined the oxidative stress effects of nicotine during pregnancy and lactation. The adverse effect of prenatal smoking exposure on human fetal development and growth has been a major public health issue. Active or passive smoking during pregnancy can result in a wide variety of adverse outcomes, including intrauterine growth retardation (IUGR), prematurity, stillbirth, and the sudden infant death syndrome. Smoking in pregnancy has also been associated with an increased risk of attention deficit and learning problems in childhood. Some studies argued that as a principal component of tobacco smoke, nicotine alone is responsible for the majority of negative reproductive outcomes. Nicotine and its major metabolite cotinine can cross the placental barrier. The level of nicotine in fetal tissues was found to be equal to or greater than the plasma nicotine level in the mothers. The oxidative stress induce by nicotine has been increasingly postulated as a major contributor to endothelial dysfunction. A large body of research has investigated the potential role of antioxidant nutrients in the prevention of endothelial dysfunction in women. Therefore, the present study was undertaken to assess the potential benefit of antioxidant supplementation on markers of placental oxidative stress in an in vitro model of endothelial dysfunction induced by nicotine, since it was previously found that nicotine is able to trigger the placental secretion of stress molecules. In this regard, we evaluated the effects of vitamin C, vitamin E and N-acetylcysteine (NAC), alone or in combination, in placental villi culture after exposure to nicotine. The effect of antioxidant nutrients on trophoblast cells proliferation and vitality was also evaluated. The results obtained suggest that in a patho-physiological condition, such as endothelial dysfunction induced by nicotine, the deleterious effect of reactive oxygen species may be counteracted by an antioxidant therapy, and there is the need to investigate the optimum dosing and timing of antioxidants administration, since an inappropriate antioxidant treatment in pregnant women may have deleterious consequences, reducing placental cells proliferation until to cell death

Group B streptococcus late-onset disease,contaminated breast milk and mothers persistently GBS negative: Report of 3cases

Background: Human milk is fundamental for its nutritional properties and to protect newborns, but it is not sterile and can sometime transmit bacteria. Few anecdotal cases suggest that breast milk could be a possible source of group B Streptococcus (GBS) late onset disease, although the pathogenesis is not entirely understood. Case presentation: We report 3 cases of GBS late onset disease in full-term newborns. Fresh breast milk cultures yielded GBS, but mothers of neonates had no signs of mastitis and remained persistently GBS negative at rectovaginal site. Conclusions: Breast milk containing group B Streptococcus can be a risk factor for late onset disease. The persistent negative maternal GBS status supports the assumption that newborns, colonised in the throat, could be the initial source of GBS, while the mammary gland could act as a GBS replication site. It is unclear whether a low bacterial load may represent only contamination rather than true milk infection

Etiopathogenesis and pharmacological prevention of a type-2 diabetes model in male mice

We describe a stress-derived type-2 diabetes model in male mice, and formulate new hypotheses on how the model was induced, how diabetes-like alterations were prevented through specific pharmacological treatments, and how its possible neuroendocrine pathogenesis could be hypothesized. Pregnant females arrived in our laboratory on their 14th day of conceptional age. After birth, control mice never showed any apparent behavioral-metabolic-endocrine alterations. However, application of postnatal stress (brief mother deprivation, plus sham injection, daily from birth to weaning), was followed in adult male mice by two series of diabetes-like alterations. Some alterations (e.g., body overweight, immune, neurophysiologic, neurobehavioral alterations) were selectively prevented by opioid antagonist naloxone daily administered during nursing period. The aforementioned alterations plus several others (e.g., hyperglycemia, neuroendocrine alterations) were prevented by administration of specific antisense oligodeoxinucleotide, which modulated synthesis-hyperfunction of proopiomelanocortin-derived corticotropin (ACTH)-corticosterone and endorphins in the pituitary. Surprisingly, together with metabolic alterations, enduring increment of neurophysiologic/neurobehavioral brain performances were observed, accompanied by energy compensative reactions, and brain mitochondria hyperfunction. Thus, increased glycemia/lipidemia appeared to furnish fuel necessary to cope with increased request of energy. Diabeteslike alterations were accompanied by enduring hyperfunction of opioid- and ACTH-corticosterone-endogenous structures in the brain, which were apparently due to failure of negative feedback hormone mechanisms in the pituitary, for the control of the hypothalamus-pituitary-adrenal axis. In conclusion, for the first time we can hypothesize that a diabetes-like syndrome is produced by enduring hyperfunction of two proopiomelanocortin-dependent endogenous systems (brain opioid- and ACTH-corticosterone systems), following failure of pituitary feedback hormonal control, after complex stress procedures

Postnatal Stress Procedures Induce Long-Term Endocrine and Metabolic Alterations Involving Different Proopiomelanocortin-Derived Peptides

The term stress is still a sort of shadowy anonimity. According to Hans Selye (1976), “Stress is the nonspecific response of the body to any demand”. A stressor is an agent that produces stress at any time. The general adaptation syndrome represents the chronologic development of the response to stressors when their action is prolonged. It consists of three phases: the alarm reaction, the stage of resistance and the stage of exhaustion. The manifestations of the alarm reaction included the secretion of adrenocorticotropic hormone (ACTH), corticoids and catecholamines, thymico-lymphatic involution, eosinopenia and peptic ulceration (Selye, 1976). The definition of the diseases of adaptation or stress-induced maladies is still cause of debate. The diseases of adaptation depend primarily upon an excessive or inappropriate response to indirect pathogens. Included are all "psychosomatic" diseases, allergies and other immunologic responses, as well as excessive inflammatory reactions. However, at least two topics still need further definition- first, connections between the type of stress and the type of disease and ,second, qualitative and quantitative definition of stress