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EN
Objective: The aim of the study was to present the biopsychosocial effects of foetal alcohol syndrome among the children from the Interventional Care Facility in Otwock in the years 2012–2015. Material and methods: We analysed medical records from the years 2012 to 2015. Medical documentation consisted of the child’s stay record, psychological diagnosis, maternal interview, social interview, a round check report, medical assessment and consultation records, neurological examination reports and physiotherapist reports. The study included medical documentation of 18 girls (29%) and 44 boys (71%). In total, 62 children aged between 3 days and 1 year were included in the study group. Results: Consumption of alcohol during pregnancy is still declared by many women (69%), including 44% of mothers consuming alcohol throughout the duration of pregnancy. All children in the Interventional Care Facility had at least 2 dysmorphic facial features. Sucking dysfunction, which caused difficulty when feeding, was observed in 59 children, and dysaesthesia – in 56 children. Children with foetal alcohol syndrome were very tearful, experienced tensions (58 children), hyperactivity (59 children) as well as sleep disorders (60 children). They frequently experienced emotional disorders (60 children) and problems with establishing contact with other people (44 children). Conclusions: It was found that alcohol has teratogenic effects on the developing foetus. Any amount of alcohol consumed by a pregnant woman can cause damage to the foetus. Foetal exposure to alcohol leads to multiple disorders that occur not only in the biological, but also in the psychological sphere. The study confirmed that children with foetal alcohol syndrome suffer from multiple health problems and have difficulty functioning in society due to their “otherness”.
PL
Cel pracy: Celem pracy było przedstawienie biopsychospołecznych skutków występowania płodowego zespołu alkoholowego wśród podopiecznych Interwencyjnego Ośrodka Preadopcyjnego w Otwocku w latach 2012–2015. Materiał i metoda: W badaniu wykorzystano metodę analizy dokumentacji medycznej z lat 2012–2015. Dokumentacja medyczna składała się z karty pobytu dziecka w ośrodku, diagnozy psychologicznej, wywiadu z matką, wywiadu socjalnego, karty obchodów, oceny badań i konsultacji lekarskich, karty badania neurologicznego oraz oceny rehabilitanta. Badanie objęło dokumentację medyczną 18 dziewcząt (29%) i 44 chłopców (71%). Łącznie grupę badaną stanowiło 62 dzieci w przedziale wiekowym od 3. dnia życia do 1. roku życia. Wyniki: Do spożywania alkoholu w ciąży przyznaje się nadal wiele kobiet (69%), w tym znaczna część do spożywania alkoholu przez cały okres trwania ciąży (44%). Wszystkie dzieci znajdujące się w Interwencyjnym Ośrodku Preadopcyjnym miały przynajmniej 2 dysmorfie twarzy. Zaburzony odruch ssania, który utrudniał jedzenie, miało 59 dzieci, a zaburzenie czucia – 56 dzieci. Dzieci z płodowym zespołem alkoholowym były bardzo płaczliwe, nadpobudliwe (59 dzieci), miały stany napięcia (58 dzieci), a także występowały u nich zaburzenia snu (60 dzieci). Bardzo często pojawiały się u nich zaburzenia emocjonalne (60 dzieci) oraz problemy z nawiązaniem kontaktu z innymi ludźmi (44 dzieci). Wnioski: Stwierdzono, że alkohol ma teratogenne działanie na rozwijający się płód. Każda ilość alkoholu spożywanego przez ciężarną może uszkodzić płód. Konsekwencją ekspozycji płodu na alkohol są liczne zaburzenia, nie tylko w sferze biologicznej, ale także psychicznej. Przeprowadzone badania potwierdziły, że dzieci z płodowym zespołem alkoholowym mają bardzo dużo problemów zdrowotnych i trudności w funkcjonowaniu w społeczeństwie, spowodowane przez ich „inność”.
EN
The well established and characterized animal model for the human demyelinating autoimmune disease mulitple sclerosis (MS) is known as experimental autoimmune encephalomyelitis (EAE). EAE is clinically characterized by focal areas of inflammation and demyelination and an infiltrate composed of large numers of lymphocytes and macrophages, often found in a perivascular localization but also throughout the central nervous system (CNS). Active immunization of mice with several different protein components of myelin, including myelin basic protein (MBP), proteolipid protein (PLP) and myelin oligodendrocyte glycoprotein (MOG), are capable of eliciting an immune response resulting in the quintessential symptoms of EAE: ascending paralysis involving the tail and then the limbs. Depending on this mouse strain and myelin antigen utilized, the disease course can be acute or chronic relapsing, characterized by a rapid onset of hind limb weakness that commonly progresses to paralysis, followed by spontaneous remission starting 7-10 days after the initial appearance of symptoms. EAE can also be induced passively by the adoptive transfer of in vitro activated CD4+ T cell clones or lines, typically of the Th1 phenotype, into irradiated susceptible recipients. The mechanisms involved in the cellular pathogenesis leading to paralysis and demyelination have been extensively studied and are primarily mediated by CD4+ T cells of the Th1 phenotype, with specificity for myelin antigens. Following activation, Th1 CD4 T cells produce in abundance the inflammatory cytokine TNF-, IFN- and lymphotoxin-alpha (LT-alpha, also known as TNF-beta). IFN-gamma production is highly correlated with encephalitogenicity and may contribute to disease by up-regulation of adhesion molecules on endothelial cells, facilitating migration of lymphocytes into the CNS; by induction of MHC class I and MHC class II molecules on astrocytes, microglial cells and brain endothelium, facilitating Ag presentation in the CNS; and by activation of macrophages, leading to production of nitric oxide, a potent cytotoxic molecule. TNF-alpha and LT-alpha are both members of the TNF family of molecules and cause cell death by apoptosis following interaction with their counter-receptors, the TNFR1 and TNF2, leading to a cascade of proteolytic events culminating in the blebbing of the cytoplasmic membrane, nuclear condensation and DNA fragmentation. Consequently, the production of TNF-alpha and LT-alpha by Th1 clones has been correlated with encephalitogenic potential and Abs to both prevents EAE upon transfer of encephalitogenic clones. Even though substantial evidence exists for the role of inflammatory cytokines in the pathogenesis of EAE, other mechanisms of myelin destruction are thought to exist. To date, many reports have implicated a role for the cell death-inducing ligand pair Fas and Fas ligand (FasL).
EN
Idiopathic pulmonary fibrosis (IPF) is a devastating disease with an almost universally terminal outcome. In recent years much insight has been gained into the pathogenesis of IPF from both a bleomycin mice-model as well as ex vivo human tissue studies. Alveolar damage and inflammation of unknown etiology, eventually leading to interstitial fibrosis, characterize IPF. Apoptosis has emerged as an important factor in the pathogenesis of IPF. This review will outline the current understanding of the immunological and molecular mechanisms underlying IPF, and discuss new therapeutic strategies.
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