No description available.

No description available.

A brainstem-related abnormality in respiratory control appears to be one of the most compelling mechanisms for sudden infant death syndrome (SIDS). The elements calcium, copper, iron, potassium, magnesium, sodium, phosphorus, sulfur, and zinc were analyzed by inductively coupled plasma atomic emission spectroscopy in the brainstem of 30 infants who died from SIDS and 10 infants who died from other causes (control). No differences were found between SIDS and control for any element except for more calcium in the SIDS group. A multivariate analysis of the data failed to group the majority of SIDS and control subjects in different clusters. Further research is required to determine the biological significance of the higher calcium found in the SIDS group.,

Sudden Infant Death (SIDS) has been associated with medium-chain acyl-CoA dehydrogenase (MCAD) deficiency, an inborn error of fatty acid oxidation. Blood and tissue samples from a large cohort of SIDS victims were analyzed for the presence of dodecanoic acid (C₁₂) by gas chromatography. A subgroup of these cases had a significantly higher blood concentration than age-matched controls, suggesting MCAD deficiency. An animal study using Sprague-Dawley rats was done to mimic the effects of MCAD deficiency. Significantly increased blood concentrations of dodecanoic acid were observed. Decreased values in heart and liver were puzzling findings. The data indicate that dodecanoic acid is a blood marker for MCAD deficiency.

Thesis (MScMedSc)--University of Stellenbosch, 2011. / ENGLISH ABSTRACT: Sudden Unexpected Death in Infancy (SUDI) refers to any such sudden demise in a child. If the child dies while asleep within the first year of life, and if no conclusive cause of death can be ascertained by means of complete autopsy and investigation into the circumstances surrounding death, including visit of the death scene, such a case is classified as one of Sudden Infant Death Syndrome (SIDS). By South African law, a full medico-legal autopsy is mandated in cases where the cause of death is not evident – including cases of possible SIDS. There can be little doubt that viral infection can be a cause of death in cases of supposed SUDI. At the Tygerberg medico-legal (forensic) laboratory, the evaluation of lung tissue for the presence of fatal viral lung infections forms part of the institutional protocol for the examination of SUDI cases. Lung samples of these SUDI cases are routinely tested for the presence of Cytomegalovirus (CMV), adenovirus and respiratory syncytial virus (RSV) by means of shell vial cultures. In a retrospective pilot study of 366 SUDI case files from Tygerberg Hospital, Western Cape, from 2004 – 2006, it was evident that in only 13.9% of possible SIDS cases, positive results for one or more of the aforementioned viruses were obtained. We hypothesise that the current method of virus detection, together with other factors such as the interval between death and post mortem examination, transport time of the specimens to the laboratory etc. might not be optimal to give a realistic picture of death in infancy caused by viral pulmonary infection. As other test modalities exist for the diagnosis of pulmonary viral infections, these methods were compared in terms of positive yield and association with viral pneumonitis, keeping the cost and time needed for each assay in mind. A total of 82 samples were collected over an 8 month period and routine shell vial cultures were done, followed by real-time Polymerase Chain Reaction (PCR) and immunohistochemical (IHC) staining of the lung sections with consensus pathology opinion. As expected, the real-time PCR method was much more better suited for identifying positive samples than shell vials (35% vs. 3.7% respectively). IHC staining also aided the pathologist in diagnosing viral infections microscopically. We expect the findings to be instrumental in streamlining not only our institutional SIDS investigation protocol, but also the development of a standardised national SIDS investigation protocol. / AFRIKAANSE OPSOMMING: “Sudden Unexpected Death in Infancy” (SUDI) verwys na enige skielike sterfte van ‘n kind. Indien die kind sterf tydens sy/haar slaap periode en geen oortuigende oorsaak van dood bepaal kan word deur middel van ’n volledige nadoodse ondersoek en ondersoek na die omstandighede tydens die dood, insluitend ’n besoek aan die doodstoneel nie, word so ’n geval as Wiegiedood (SIDS) geklassifiseer. SuidAfrikaanse wetgewing vereis ’n volledige medies-geregtelike nadoodse ondersoek in gevalle waar die oorsaak van dood onbekend is – insluitend gevalle van moontlike Wiegiedood. Daar is min twyfel dat virusinfeksie ‘n oorsaak van, of bydraende faktor tot dood kan wees in gevalle van moontlike SUDI. By die Tygerberg forensiese laboratorium vorm die evaluasie van long weefsel vir die teenwoordigheid van dodelike virusinfeksies deel van die institusionele protokol vir die ondersoek van SUDI gevalle. Long monsters van hierdie SUDI gevalle ondergaan roetine toetse vir die teenwoordigheid van sitomegaalvirus, respiratoriese sinsitialevirus en adenovirus deur middel van selkulture (“shell vial cultures”). In ‘n retrospektiewe steekproef van 366 SUDI gevalle by Tygerberg Hospitaal, Wes-Kaap van 2004 – 2006, is bevind dat in slegs 13.9% van moontlike SUDI gevalle die teenwoordigheid van een of meer van bogenoemde virusse bevestig kon word. Ons hipotese is dat hierdie metode van virus deteksie, tesame met ander faktore soos die tydsinterval tussen dood en nadoodse ondersoek, tyd om monsters na die laboratorium te vervoer ens. moontlik nie optimaal is om ‘n realistiese beeld van dood in babas as gevolg van pulmonale virusinfeksie te gee nie. Aangesien ander toets modaliteite bestaan vir die diagnose van pulmonale virusinfeksies, is hierdie metodes vergelyk in terme van positiewe opbrengs en assosiasie met virale pneumonitis, teen ’n agtergrond van die koste en tyd benodig per toets. ’n Totaal van 82 monsters is oor ‘n 8 maande periode versamel en roetine selkulture is gedoen, gevolg deur “real-time” Polimerase Ketting Reaksie (PKR), asook immunohistochemiese (IHC) kleuring van long snitte met patologiese verslae. Soos vermoed, is gevind dat die real-time PKR metode baie meer akkuraat is om positiewe monsters te identifiseer as roetine selkulture (35% vs 3.7% onderskeidelik). IHC kleuring het ook mikroskopiese diagnose van virale infeksies deur die patoloog vergemaklik. Ons verwag dat hierdie bevindinge grootliks kan bydra in die vaartbelyning van ons institusionele SIDS ondersoek protokol, asook in die ontwikkeling van ’n gestandaardiseerde nasionale SIDS ondersoek protokol.

Wong Yin. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1999. / Includes bibliographical references (leaves [110]-126). / Abstracts in English and Chinese. / ABSTRACT --- p.VI / ACKNOWLEDGEMENTS --- p.X / GLOSSARY --- p.XI / Chapter CHAPTER 1 --- INTRODUCTION AND LITERATURE REVIEW --- p.1 / Chapter 1.1 --- Sudden infant death syndrome --- p.1 / Chapter 1.1.1 --- Definition --- p.1 / Chapter 1.1.2 --- Epidemiology of sudden infant death syndrome --- p.1 / Chapter 1.1.3 --- Pathologic findings --- p.5 / Chapter 1.1.4 --- Theories of causation --- p.6 / Chapter 1.1.5 --- Associations of SIDS with temperature and hyperthermia --- p.8 / Chapter 1.1.6 --- Associations of sudden infant death syndrome with infection --- p.11 / Chapter 1.1.7 --- Association of sudden infant death syndrome with sleep state --- p.13 / Chapter 1.2 --- Overview of cytokines --- p.15 / Chapter 1.2.1 --- Definition --- p.15 / Chapter 1.2.2 --- Classification of cytokines --- p.15 / Chapter 1.2.3 --- Biological activities --- p.16 / Chapter 1.2.4 --- Cytokines and temperature --- p.20 / Chapter 1.2.5 --- Cytokines and infection --- p.22 / Chapter 1.2.6 --- Cytokines and smoking --- p.23 / Chapter 1.2.7 --- Cytokines and sleep/arousal --- p.23 / Chapter 1.3 --- Hypothesis and aims of the study --- p.27 / Chapter CHAPTER 2 --- MATERIALS AND METHODS --- p.28 / Chapter 2.1 --- Overview of methods in piglet experiments --- p.28 / Chapter 2.2 --- Pilot study design --- p.30 / Chapter 2.2.1 --- Study Groups --- p.30 / Chapter 2.2.2 --- Temperature controller --- p.33 / Chapter 2.2.3 --- PowerLab system --- p.34 / Chapter 2.2.4 --- Experimental set up --- p.36 / Chapter 2.2.5 --- Provisional ethical approval --- p.36 / Chapter 2.3 --- Problems and results of pilot experiments --- p.37 / Chapter 2.3.1 --- What is baseline body temperature of neonatal rat? --- p.38 / Chapter 2.3.2 --- What type of anaesthesic agent to use? --- p.39 / Chapter 2.3.3 --- What dose of ketamine to use? --- p.40 / Chapter 2.3.4 --- Dilution of ketamine --- p.41 / Chapter 2.3.5 --- Temperature calibration --- p.41 / Chapter 2.3.6 --- What is optimal neonatal rat age to use? --- p.44 / Chapter 2.3.7 --- Which method of blood collection to use? --- p.45 / Chapter 2.3.8 --- What method to raise body temperature? --- p.47 / Chapter 2.3.9 --- Summary results --- p.48 / Chapter 2.4 --- Final study design --- p.49 / Chapter 2.4.1 --- Study animal --- p.49 / Chapter 2.4.2 --- Final Study Groups --- p.50 / Chapter 2.4.3 --- Final ethical approval --- p.56 / Chapter 2.4.4 --- Muramyl dipeptide --- p.56 / Chapter 2.4.5 --- Recalibration of Temperature Controller --- p.57 / Chapter 2.4.6 --- Data collection --- p.58 / Chapter 2.4.7 --- Blood collection and Storage --- p.58 / Chapter 2.4.8 --- Study timetable --- p.59 / Chapter 2.5 --- Cytokines analysis --- p.59 / Chapter 2.5.1. --- Methods of Quantitative Enzyme Immunoassay --- p.59 / Chapter 2.5.2 --- Base theories of Enzyme-linked immunosorbent assay (ELISA) --- p.60 / Chapter 2.5.3 --- Procedure for cytokines assay --- p.61 / Chapter 2.6 --- Histology --- p.65 / Chapter 2.6.1. --- Macroscopic --- p.65 / Chapter 2.6.2. --- Microscopic --- p.65 / Chapter 2.7 --- Data handling and statistical analysis --- p.66 / Chapter CHAPTER 3 --- RESULTS --- p.67 / Chapter 3.1 --- Group (body weight) characteristics --- p.67 / Chapter 3.2 --- Serum concentration of IL- 6，IL-1 β --- p.69 / Chapter 3.3 --- Temperature --- p.78 / Chapter 3.4 --- Mortality rate --- p.80 / Chapter 3.5 --- Cardio-respiratory parameters --- p.85 / Chapter 3.6 --- Macroscopic findings at postmortem --- p.87 / Chapter 3.7 --- Histology --- p.91 / Chapter CHAPTER 4 --- DISCUSSION --- p.96 / Chapter 4.1 --- Study Model --- p.96 / Chapter 4.11 --- Core temperature of newborn rat --- p.95 / Chapter 4.12 --- Temperature calibration --- p.97 / Chapter 4.13 --- Respiratory and pulse rate measurements --- p.93 / Chapter 4.14 --- Measurement of sleep state --- p.99 / Chapter 4.2 --- Animal age and weight --- p.99 / Chapter 4.3 --- Cytokines response to heating --- p.101 / Chapter 4.4 --- Cytokine response to MDP --- p.104 / Chapter 4.5 --- "Hyperthermia, MDP and mortality" --- p.106 / Chapter 4.6 --- Further study --- p.107 / Chapter CHAPTER 5 --- CONCLUSION --- p.109 / Chapter 5.1 --- Small animal model of hyperthermia --- p.109 / Chapter 5.2 --- Hyperthermia and MDP elicit cytokine response --- p.109 / Chapter 5.3 --- Hyperthermia and MDP increase mortality rate --- p.109 / REFERENCES --- p.110 / APPENDICES --- p.A / Appendix 1: Experimental record --- p.A / Appendix 2 : Planned Study Timetable --- p.C / Appendix 3: PowerLab System --- p.E

Abstract not available

This thesis tests the hypothesis that increased neuronal cell death in SIDS infants is related to the ability of risk factors, such as prone sleeping, to expose infants to intermittent hypercapnic hypoxia (IHH). Based on the hypothesis that the NMDA system is linked to neuronal death, by way of excitotoxicity, correlations were also sought between cell death and changes in NMDA receptor (NR1) expression in brainstem nuclei controlling cardiorespiratory function. The first aim of this study was to verify that increased neuronal cell death occurs in SIDS infants. To verify a piglet model of SIDS risk factors, brainstem changes were examined in piglets exposed to IHH, and comparisons were made to changes seen in SIDS infants. The NMDA receptor was characterised in controls for both the human infant and the piglet groups. Comparisons of neuronal changes were made with SIDS infants, and piglets exposed to IHH. Non-radioactive in-situ hybridisation and immunohistochemistry were performed on formalin fixed and paraffin embedded brainstem tissue to identify markers of cell death (caspase-3, active caspase-3, and TUNEL), and to examine NR1 mRNA and protein expressions. Staining was quantified using computerised image analysis software. Eight nuclei from the brainstem medulla (caudal in piglets, and mid in infants), and two nuclei from the rostral pons (infants) were studied. The first dataset included human infants aged 1-6 months with a diagnosis of SIDS (n=15) or non-SIDS (n=10). The second dataset comprised developing piglets aged 13-14 days, with controls (n=6), against those exposed to IHH for 2 (n=6) or 4 (n=5) days. Increased neuronal cell death was not verified in the SIDS infants, but abnormalities in NR1 expression were present in selected nuclei of the medulla. Piglets exposed to IHH had increased neuronal cell death and changes in NR1 in selected nuclei of the medulla. There was also a positive correlation between increased cell death and high NR1 levels. Preliminary data showed that SIDS infants who usually slept prone had some differences in NR1 compared to those who did not usually sleep prone. From these findings, it was concluded that IHH may underlie the abnormalities in NMDA receptor expression that are present in the brainstem of SIDS infants. Although IHH can induce an increase in neuronal cell death, its significance in the aetiology of SIDS is not known. In piglets, IHH induced cell death correlated with high NMDA expression in some brainstem nuclei, supporting the hypothesis that excitotoxicity may be involved in the mechanism for cell death. Moreover, this thesis presents for the first time, �preliminary pathological proof� of an association between prone sleeping and abnormal NMDA receptor expression in SIDS infants.

ABSTRACT Objective The aim of this study was to determine if and what kind of scientific evidence there is for the advice that breast-feeding can reduce the risk of sudden infant death syndrome (SIDS). The aim was to investigate research on the subject published in the last 15 years. Method A systematic review without meta-analysis with relevant original articles published in the last 15 years. Main results After searching for articles 26 relevant articles were used for this study and two were excluded because of poor quality. Mixed results were shown on breast feeding and the risk of SIDS. Breast-feeding seems to have some protective effect but can’t be separated from known risk factors of SIDS. Plain language summary Breast feeding can be regarded as a preventive measure against SIDS. However socioeconomic factors may play a bigger part than breast feeding alone in the protection against SIDS. Mothers should be given the advice to breast feed as a preventive measure of SIDS. The authors suggest that more research is needed. / ABSTRACT Syfte Syftet med denna studie är att undersöka om och i så fall vilket vetenskapligt stöd det finns för rådet om amning som preventiv åtgärd mot plötslig spädbarnsdöd (sudden infant death syndrome, SIDS). Studien syftar till att undersöka de senaste 15 årens forskning i ämnet. Metod En systematisk litteraturstudie utan meta-analys med relevanta originalartiklar publicerade de senaste 15 åren. Resultat Antalet relevanta artiklar var 26, två artiklar exkluderades på grund av låg kvalitet. Sex kategorier relaterade till amning kunde identifieras. De granskade studierna har visat varierande resultat gällande amningens inverkan på risken för SIDS. Amningen har visats ha skyddande effekter som inte kan särskiljas från kända riskfaktorer för SIDS. Slutsats Amning kan fungera som en preventiv åtgärd mot SIDS. Dock verkar socioekonomiska faktorer ha en större roll än amning enskilt för att ge ett skydd mot SIDS. Rådet om att amning skyddar mot SIDS är adekvat och denna litteraturöversikt kan ge ökad kunskap om olika aspekter av amningens effekter. Författarna menar att det finns ett behov av ökad kunskap inom detta område.

Syfte: Att utifrån vetenskaplig litteratur beskriva föräldrars upplevelse av stöd generellt och av distriktssköterskan specifikt, efter att ha förlorat ett barn i plötslig spädbarnsdöd. Ett ytterligare syfte var att beskriva de ingående artiklarnas urvalsmetod. Metod: Litteratursökningen genomfördes i databaserna Medline och Cinahl samt via manuell sökning. Tio artiklar som mötte inklusionskriterierna granskades. Resultat: De flesta föräldrarna ansåg att de fick bra stöd i det akuta skedet och på sjukhuset. Mödrar fick något mer stöd än fäder. Det viktigaste stödet efter att ha lämnat sjukhuset var stödet från maken eller makan. Stödet från släkt, vänner och bekanta kunde antingen underlätta eller försvåra sorgearbetet. Upplevelsen av hjälp från stödgrupper berodde på vilken fas i sorgeprocessen som föräldern var i. Generellt fick få föräldrar stöd från distriktssköterskan även om det hade varit önskvärt. Många fäder tyckte dock att distriktssköterskan var den viktigaste stödpersonen. Majoriteten av föräldrarna önskade att distriktssköterskan kontaktade dem när de kommit hem från sjukhuset. Slutsats: En övervägande del av föräldrarna får någon form av stöd efter att ha förlorat ett barn i plötslig spädbarnsdöd. Mer utbildning för vårdpersonal önskas för att de bättre ska kunna stödja sörjande föräldrar. / Aim: based on literature review describe the parent´s experience of support in general and from the primary health nurse specifically, after the lost of a child in SIDS. A further aim was to describe the articles selection method. Method: A literature search was conducted in the databases Medline and Cinahl and through manual search. Ten articles that met the inclusions criteria were reviewed. Findings: Most parents felt that they received good support in the acute phase and in hospital. Mothers were slightly more supported than fathers. The most important support after leaving the hospital was the support from the spouse. Support from family, friends and acquaintances could either facilitate or complicate grief. The experience of help from support groups depended on the phase of the grieving process that parents were in. Generally only a few parents received support from the primary health nurse even if it had been desirable. Many fathers felt that the primary health nurse was the main support person. The majority of parents wanted the primary health nurse to contact them when they came home from the hospital. Conclusion: The majority of parents got some sort of support after losing a child in SIDS. More training for health care professionals is desired in order to better be able to support bereaved parents.