A kötődési kapcsolatok stabilitása gyermekkorban = Stability of attachment relationships in childhood

Alacsony szociális rizikójú családokkal folytatott longitudinális vizsgálatunkban elsőszülött gyermekek kötődési kapcsolatainak állandóságát ill. változását, valamint ezek feltételezett korrelátumait elemeztük. A csecsemőkorban megfigyelt anya-gyermek kötődési minőség nem bizonyult stabil mintázatnak sem 1 és 4, majd 4 és 6, sem 1 és 6 éves kor között. Az anyához való kötődés változása elsősorban a fiú gyermekeket érintette, akik egyik életkori összehasonlításban sem mutattak stabil kötődési mintázatot. A lány gyermekek csoportjában ugyakkor folytonosságot találtunk mindhárom mérési időpont között a biztonságos vs. bizonytalan anyai kötődés tekintetében. Az anya-gyermek kötődési kapcsolat kevésbé optimális irányba történő változásának hátterében a gyermek nemét (fiú) és a kumulatív környezeti stresszt (súlyos betegségek, halálozások, szeparációk, stb.) azonosítottuk rizikófaktorként. Az anyához való kötődéssel ellentétben az apa-gyermek kötődési biztonság jelentős stabilitást mutatott 1,5 és 7,5 éves kor között. Kimutattuk, hogy a 6 éves korban anyjukhoz biztonságosan kötődő gyermekek jobbak az érzelmek felismerését és megnevezését vizsgáló feladatban, míg az apához való kötődés minősége ezt nem befolyásolta. Bővítve korábbi felfedezésünket a gyermekek DRD4 genotípusa és az 1 éves kori dezorganizált (D) kötődés kapcsolatáról, jelen kutatásban kimutattuk, hogy ez a genotípus a 4 és 6 éves kori D kötődés megjelenésében, valamint életkori állandóságában is szerepet játszik. | The present research investigated continuity and change in attachment relationships of firstborn children from infancy to childhood in a low-social-risk sample. For the whole sample, no longitudinal stability of mother-child attachment security was found from 1 to 4, from 4 to 6, or from 1 to 6 years. Changes in mother-child attachment mainly concerned boys, who did not show stable attachment patterns over time in any age contrasts. In the group of girls, however, security of attachment to the mother proved stable across all assessment periods. Male sex and cumulative life stress (serious illnesses, major losses, separations, etc.) were identified as risk factors for unfavourable change in mother-child attachment from infancy to childhood. In contrast to mother-child attachment, significant continuity in father-child attachment security was found from 1.5 to 7.5 years. We showed that 6-year secure attachment to the mother was associated with children?s better performance in recognition and labelling of emotions, while quality of attachment to the father was not related to the ?emotion task?. Expanding our previous findings on the association between child DRD4 genotype and 1-year disorganised (D) attachment, the present study showed that this genotype also influences the occurrence of D attachment both at 4 and 6 years of age, and its stability over early childhood

Az értelmi fejlődés, a viselkedésszervezés egyidejű és longitudinális összefüggésmintázatai a perinatális rizikó és a környezeti feltételek függvényében: koraszülött és időre született gyerekek követése iskoláskorig = Concurrent and longitudinal patterns of mental and behavioural development in function of perinatal risk and environmental background: follow-up of preterm and full-term children into school age

Előző OTKA pályázatunk keretében születésüktől 4 éves korig követtük egy mérsékelt rizikószintű koraszülött gyerekekből álló csoport valamint egy időre született, egészséges csoport fejlődését. A jelen pályázat lehetővé tette a longitudinális kutatás újabb adatgyűjtési hullámát a gyerekek 6-7 éves korában, és a korábbi fejlődési adatok fölhasználásával mód nyílt a fejlődés hosszabb távon érvényesülő összefüggéseinek elemzésére. 4 éves korra úgy tűnt, hogy a koraszülött csoport javarészt behozta a korábbi fejlődési vizsgálatok alkalmával tapasztalt lemaradását, ez a tendencia azonban nem folytatódott tovább. 6 éves korban - noha az átlagos értékek az értelmi fejlődés minden vizsgált mutatójában a normál zónába tartoznak - az időre született egészséges csoport teljesítményével összehasonlítva a koraszülöttek markánsan alul maradtak. A teljesítmények egyidejű és longitudinális összefüggés-mintázatainak elemzése megfontolandó tanulságokkal szolgált. Tovább dolgoztunk az anya-gyerek interakcióról valamint a vizsgálati helyzetekről korábban készült videofelvételeken is. A 4 éves korban rögzített interakciók elemzése a korábbi megfigyelésekkel szemben a koraszülött gyerekeket megkülönböztető viselkedéses jellemzőket azonosított, az anyák viselkedése viszont már nem tért el a két csoportban. Megfigyeléses adataink alátámasztják a korábbi kutatásokban tapasztaltakat, amelyek szerint koraszülött gyerekeknél a temperamentum és a mentális fejlődés szoros kapcsolatban áll. | In our previous research a group of moderate-risk preterm infants and a comparison group of healthy full-term infants had been followed from birth through 4 years. The present grant made a new wave of data collection possible at the age of 6-7 years. It also gave us an opportunity to analyse longer-term developmental patterns using data from earlier stages of the children's growth. By 4 years the preterm children appeared to have caught up, overcoming the developmental delays found at the earlier assessments. However, the promising trend did not seem to continue. Although at age 6 the mean scores of the preterm sample on all outcome measures fell within the normal range, their performances lagged behind the performances of the non-risk comparison group. The analysis of the concurrent and longitudinal patterns of performances gave us further insights to the long-term impact of premature birth. In addition to the analysis of the developmental data, we continued working on the videotapes of mother-child interactions recorded in the previous years. At 4 years of age the behaviours of the preterm children had more distinct characteristics than in infancy, while the differential behaviours found earlier in their mothers were not present any more. Our observational data corroborate the strong link between the mental development and temperament in preterm children reported by several authors

Guidelines for the use and interpretation of assays for monitoring autophagy

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field

Guidelines for the use and interpretation of assays for monitoring autophagy

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field

Guidelines for the use and interpretation of assays for monitoring autophagy

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field

Erratum to: Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (Autophagy, 12, 1, 1-222, 10.1080/15548627.2015.1100356

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Guidelines for the use and interpretation of assays for monitoring autophagy

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field