Činnost nervového systému je založena na aktivitě jednotlivých neuronálních okruhů. Správná funkce těchto okruhů je výsledkem společného vlivu genetických a epigenetických faktorů, které jsou zodpovědné za vývoj struktury i funkce. Poměr vlivu obou faktorů závisí na typu daného neuronálního okruhu a na stádiu jeho vývoje. Význam autonomní buněčné diferenciace (založené hlavně na genetických faktorech) a buněčných interakcích (podmíněných převážně epigenetické faktory) vyplývá z vlastností embryonální tkáně samé a závisí i na působení zevního prostředí (faktory výživy, zásobení kyslíkem, senzorická a sociální zkušenost, učení). Podobně jako u jiných altriciálních živočichů, není mozek člověka při narození ještě plně vyvinut. Nervové okruhy vznikající vzájemným rozpoznáváním a interakcí nervových buněk v prenatálním období jsou jen přibližnou formou konečného zapojení. V dalším vývoji je tento systém zapojení postupně upřesňován (vylaďován) tak, aby si jednotlivé články neuronálních okruhů přesně funkčně odpovídaly. Neuroplastické pochody, které vývoj podmiňují, mohou být v určité fázi modulovány faktory výživy, intenzitou nebo modalitou senzorických podnětů, na základě sociálních zkušeností. nebo působením některých patologických podnětů. Podle klinických nálezů se většina negativních změn v dalším období vývoje opět vyrovnává. Pouze intenzivní nebo dlouhodobé alterační faktory mohou zanechat trvalé změny stavby a funkce neuronálních okruhů a projevit se příznaky minimálního mozkového poškození. Těmi jsou např. poruchy pozornosti a snížení schopnosti interakce s prostředím. Důsledky v podobě isolace dítěte od okolí jsou často spojené s vážnými poruchami učení. Vzhledem k vysoké aktivitě neuroplastických procesů v období vývoje je vhodné připadnou nutriční, psychosociální nebo psychomotorickou rehabilitaci postiženého dítěte zahájit co nejdříve.
Performance of the nervous system is based on the actions of distinct neuronal circuits. Correct activity of these circuits results from the joint effects of genetic and epigenetic factors, responsible for the development of structure and function. The relative contribution of each of them varies among given neuronal circuits and the stage of their development. The significance of cell autonomous differentiation (related mostly to genetic factors) and cellular interactions (based on both genetic and epigenetic factors) results both from the features of the embryonic tissue and the activity of environmental factors (nutrition, availability of oxygen, sensory and social experience, learning). The human brain (as well as brain of other altricial organisms) is not fully developed at birth. Neuronal circuits that result from the cell recognition events during the prenatal development only roughly approximate the final wiring. The initially coarse pattern of connections is subsequently refined (tuned) to match precisely the presynaptic neurons to their appropriate target cells. These neuroplastic processes can be modulated at the specific period of time by nutritional factors, sensory experience, social interaction or pathological events. Clinical observations indicate that most of the alterations eventually recover. However, intensivve or long-termed deprivation factors may result in permanent changes of the structure and functions of neuronal circuits and bring about variety of minimal brain dysfunction-type syndromes and ultimately aiiect attentional processes and interactions of the organism with the environment. Considering the high activity of neuroplastic processes during the development, it is advisable to start the nutritional, psychosocial, and psychomotor rehabilitation of the child in the early infancy.
In the human, placental structure is closely related to placental function and consequent pregnancy outcome. Studies have noted abnormal placental shape in small-for-gestational-age infants which extends to increased lifetime risk of cardiovascular disease. The origins and determinants of placental shape are incompletely understood and are difficult to study in vivo. In this paper, we model the early development of the human placenta, based on the hypothesis that this is driven by a chemoattractant effect emanating from proximal spiral arteries in the decidua. We derive and explore a two-dimensional stochastic model, and investigate the effects of loss of spiral arteries in regions near to the cord insertion on the shape of the placenta. This model demonstrates that disruption of spiral arteries can exert profound effects on placental shape, particularly if this is close to the cord insertion. Thus, placental shape reflects the underlying maternal vascular bed. Abnormal placental shape may reflect an abnormal uterine environment, predisposing to pregnancy complications. Through statistical analysis of model placentas, we are able to characterize the probability that a given placenta grew in a disrupted environment, and even able to distinguish between different disruptions.
- MeSH
- Umbilical Arteries physiology MeSH
- Models, Biological * MeSH
- Embryonic Development physiology MeSH
- Neovascularization, Physiologic physiology MeSH
- Oxygen metabolism MeSH
- Humans MeSH
- Organogenesis physiology MeSH
- Placenta embryology MeSH
- Placentation MeSH
- Computer Simulation MeSH
- Models, Statistical MeSH
- Stochastic Processes MeSH
- Pregnancy MeSH
- Check Tag
- Humans MeSH
- Pregnancy MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
BACKGROUND: Cerebral oxygenation (crSO2) monitoring is increasingly used in high-risk infants. Monochorionic twins suffer from specific fetal pathologies that can affect cerebral hemodynamics. Limited data are available on crSO2 and blood flow patterns in this population after birth. OBJECTIVE: To evaluate crSO2 changes in preterm monochorionic and dichorionic twins during the first 72 h of life. METHODS: Near-infrared spectroscopy was used to measure crSO2 in 62 infants from 31 twin pregnancies <32 weeks of gestation. The study group was divided into 4 subgroups: donor (1) and recipient (2) monochorionic twins (with twin-twin transfusion syndrome), fetal growth restriction (FGR) infants (3) and twins without fetal compromise (4). RESULTS: There was significant difference in birth weight (p < 0.001) among 4 subgroups. We observed significant variation in crSO2 among the subgroups using mixed model analysis (p < 0.001). The recipient twins exhibited the lowest crSO2 (mean ± SE) throughout the study period (76 ± 0.3%), whereas the FGR and donor twins presented with the highest values (86 ± 0.3% and 83 ± 0.4% respectively). We found no statistically significant differences in neonatal mortality and morbidity among subgroups. CONCLUSION: Our study revealed significant correlation between crSO2 values postnatally and underlying fetal pathology in monochorionic and dichorionic preterm twins.
- MeSH
- Spectroscopy, Near-Infrared MeSH
- Chorion MeSH
- Twins, Dizygotic * MeSH
- Fetofetal Transfusion etiology MeSH
- Oxygen analysis MeSH
- Humans MeSH
- Cerebrovascular Circulation * MeSH
- Infant, Premature MeSH
- Infant, Newborn MeSH
- Birth Weight MeSH
- Prospective Studies MeSH
- Fetal Growth Retardation etiology MeSH
- Pregnancy, Twin * MeSH
- Pregnancy MeSH
- Fetal Development MeSH
- Check Tag
- Humans MeSH
- Infant, Newborn MeSH
- Pregnancy MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Observational Study MeSH
- Research Support, Non-U.S. Gov't MeSH
Our present focus on the hypoxic immature heart is driven by clinical urgency: cyanotic congenital cardiac malformations remain the single largest cause of mortality from congenital defects and ischemic heart disease is no more the disease of the fifth and older decades but its origin as well as risk factors are present already during early ontogeny. Moreover, the number of adult patients operated for cyanotic congenital heart disease during infancy steadily increases. This group approaches the age of the rising risk of serious cardiovascular diseases, particularly ischemic heart disease. Experimental results have clearly shown that the immature heart is significantly more tolerant to oxygen deficiency than the adult myocardium. However, the mechanisms of this difference have not yet been satisfactorily clarified; they are likely the result of developmental changes in cardiac energy metabolism, including mitochondrial function. The high resistance of the newborn heart cannot be further increased by ischemic preconditioning or adaptation to chronic hypoxia; these protective mechanisms appear only with decreasing tolerance during development. Resistance of the adult myocardium to acute oxygen deprivation may be significantly influenced by perinatal hypoxia. These results suggest that the developmental approach offers new possibilities in the studies of pathogenesis, prevention and therapy of critical cardiovascular diseases.
- MeSH
- Energy Metabolism MeSH
- Financing, Organized MeSH
- Adaptation, Physiological MeSH
- Hypoxia metabolism physiopathology MeSH
- Ischemic Preconditioning, Myocardial MeSH
- Cardiovascular Diseases metabolism physiopathology prevention & control MeSH
- Oxygen metabolism MeSH
- Humans MeSH
- Myocardium metabolism MeSH
- Sex Factors MeSH
- Heart physiopathology growth & development MeSH
- Mitochondria, Heart metabolism MeSH
- Age Factors MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Male MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Review MeSH
- Keywords
- volné kyslíkové radikály,
- MeSH
- Acute Disease MeSH
- Oxygen MeSH
- Humans MeSH
- Pulmonary Embolism MeSH
- Hypertension, Pulmonary etiology physiopathology MeSH
- Vasoconstriction physiology MeSH
- Free Radicals MeSH
- Check Tag
- Humans MeSH
- Publication type
- Review MeSH
A broad spectrum of conditions including neuropathic pain, complex regional pain syndrome (CRPS) and fibromyalgia, have been implicated as causes of chronic pain. There is a need for new and effective treatments that patients can tolerate without significant adverse effects. One potential intervention is hyperbaric oxygen treatment (HBOT). The case reported here is unique in describing repeated HBOT in a patient who developed recurrent post-traumatic CRPS of the lower as well as the upper limbs. In the first event, two months after distortion and abruption of the external right ankle, the patient suffered leg pain, oedema formation, mild hyperaemia, limited mobility of the ankle and CRPS Type 1. In the second event, the same patient suffered fracture-dislocation of the distal radius 1.5 years after the first injury. After the plaster cast was removed the patient developed pain, warmth, colour changes, oedema formation and limited wrist mobility with CRPS Type 1. Pharmacological treatment as well as HBOT were used with significant improvement of functional outcome in both cases. Some studies suggest that patients with a history of CRPS are more likely to develop secondary CRPS compared to the rates reported in the literature among the general population. Patients with a history of CRPS should be counselled that they may be at risk for developing secondary CRPS if they undergo surgery or sustain trauma to another extremity.
- MeSH
- Pain MeSH
- Hyperbaric Oxygenation * MeSH
- Complex Regional Pain Syndromes * etiology therapy MeSH
- Oxygen MeSH
- Humans MeSH
- Reflex Sympathetic Dystrophy * therapy MeSH
- Check Tag
- Humans MeSH
- Publication type
- Case Reports MeSH
