Sudden infant death syndrome (SIDS) BS

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Bioresource Technology 98 (2007) 1353–1358 0960-8524/$ - see front matter © 2006 Elsevier Ltd. All rights reserved. doi:10.1016/j.biortech.2006.05.029 The role of chitosan in protection of soybean from sudden death syndrome caused by Fusarium solani f. sp. glycines Benjaphorn Prapagdee a,¤ , Kanignun Kotchadat a , Acharaporn Kumsopa a , Niphon Visarathanonth b a Faculty of Environment and Resource Studies, Mahidol University, Salaya, Nakhon Pathom 73170, Thailand b Department of Plant Pathology, Faculty of Agriculture, Kasetsart University, Bang Khen, Bangkok 10220, Thailand Received 12 September 2005; received in revised form 18 May 2006; accepted 21 May 2006 Available online 7 July 2006 Abstract The in vitro antifungal properties of chitosan and its role in protection of soybean from a sudden death syndrome (SDS) were evalu- ated. Chitosan inhibited the radial and submerged growth of F. solani f. sp. glycines with a marked eVect at concentrations up to 1 mg/ml indicating antifungal property and at 3 mg/ml was able to delay SDS symptoms expression on soybean leaves for over three days after fungal inoculation when applied preventively. Chitosan was able to induce the level of chitinase activity in soybean resulting in the retar- dation of SDS development in soybean leaves. However, the SDS symptoms gradually appeared and were associated with the reduction of chitinase activity level after Wve days of infection period. These results suggested the role of chitosan in partially protecting soybeans from F. solani f. sp. glycines infection. © 2006 Elsevier Ltd. All rights reserved. Keywords: Fusarium solani; Chitosan; Sudden death syndrome; Soybean 1. Introduction Sudden death syndrome (SDS), caused by the soil-borne fungus F. solani f. sp. glycines, is an economically harmful disease of soybean (Rupe, 1989). SDS causes rapid defolia- tion of soybean, resulting in reducing both the quality and quantity of soybean product (Roy et al., 1989; Rupe, 1989). The development of SDS is favored by cool and wet rhizo- spheric conditions through the growing season (Scherm and Yang, 1996). There is no total elimination of this dis- ease because F. solani f. sp. glycines as mycelium and chla- mydospores can survive in the soil and tolerate to the unfavorable conditions (Rupe and Gbur, 1995). The use of chemical substances for controlling Fusarium pathogen, mainly methyl bromide as a broad spectrum disinfectant, has been found to be eVective (Allen et al., 2004). However, the excessive application of chemical fungicides led to increase in fungicide resistance in pathogens and a contin- ued presence of the pathogens in other areas of the Weld (Bourbos et al., 1997) as well as contamination of the envi- ronment. Additionally, the fungicides contaminated in the environment tend to accumulate in agricultural products and human body via the food chain. Chitosan (poly--(1,4)- D-glucosamine), a transformed oligosaccharide, is obtained by alkaline deacetylation of chitin, one of the most abundant natural biopolymers, that is extracted from the exoskeleton of crustaceans such as shrimps and crabs, as well as the cell Sudden infant death syndrome (SIDS) By Mayo Clinic staff Original Article:http://www.nlm.nih.gov/medline plus/suddeninfantdeathsyndrome.html Definition • Sudden infant death syndrome (SIDS) is the unexplained death, usually during sleep, of a seemingly healthy baby Definition • Most SIDS deaths occur in children between months and months of age Sudden infant death syndrome rarely occurs before month of age or after months Causes • Brain and nerve characteristics: Infants who die of SIDS may have brainstems that mature more slowly than those of other infants Myelin, a fatty substance involved in nerve signal transmission, also may develop more slowly in infants with SIDS Causes  Breathing Other research has focused on the way babies breathe while they're asleep — especially their response to low blood oxygen levels (hypoxia) Causes • Heart function Researchers continue to investigate the link between SIDS and long QT syndrome, a subtle electrical disturbance in the heart that causes sudden, extremely rapid heart rates Causes  Immunizations After reviewing the available evidence, the American Academy of Pediatrics concluded that childhood immunizations don't play a role in sudden infant death syndrome Risk factors • Male Boy babies are more likely to die of SIDS • Between month and months of age Infants are most vulnerable during the second and third months of life Risk factors • Premature or of low birth weight Your baby is more susceptible to SIDS if he or she was premature or had a low birth weight • Black, American Indian or Native Alaskan For reasons that aren't well understood, there appears to be an association between race and the risk of SIDS Risk factors • Placed to sleep on their stomachs • Babies who sleep on their stomachs are much more likely to die of SIDS than are babies who sleep on their backs • Side sleeping — because infants placed on their sides are likely to roll to their stomachs — and soft bedding have also been found to contribute to risk Risk factors  Born to mothers who smoke or use drugs Smoking cigarettes during or after your pregnancy puts your baby at considerably higher risk of SIDS Using drugs such as cocaine, heroin or methadone while you're pregnant also increases the risk Risk factors   Exposed to environmental tobacco smoke Infants exposed to secondhand smoke have a higher risk of SIDS Born during the fall or winter months More SIDS cases occur when the weather is cooler Risk factors • Overheated Some evidence suggests that babies who are overdressed, covered with multiple blankets or whose rooms are too warm are at greater risk of SIDS, especially if they're put to sleep on their stomachs Risk factors  Recently recovered from an upper respiratory infection Evidence of infection within four weeks of death is a common finding in SIDS autopsies Risk factors • Also at risk are babies whose mothers had: • Inadequate prenatal care • Placental abnormalities — such as placenta previa, a condition where the placenta lies low in the uterus, sometimes covering the opening of the cervix • Low weight gain during pregnancy • Their first pregnancy at younger than 20 years of age • Anemia • History of sexually transmitted diseases or urinary tract infections Prevention • There's no guaranteed way to prevent SIDS, but you can help your baby sleep safely Recommendations from the American Academy of Pediatrics include the following: Prevention • Put your baby to sleep on his or her back • Be sure your baby is placed to sleep on his or her back when in the care of others • Don't smoke • Select bedding carefully Prevention • Place your baby to sleep in a crib or bassinet — not in your bed • Keep your baby nearby • Consider breast-feeding • Moderate room temperature CAS E REP O R T Open Access Opitz trigonocephaly syndrome presenting with sudden unexplained death in the operating room: a case report Laura Travan 1* , Vanna Pecile 2 , Mariacristina Fertz 1 , Antonella Fabretto 2 , Pierpaolo Brovedani 1 , Sergio Demarini 1 and John M Opitz 3 Abstract Introduction: Opitz trigonocephaly C syndrome (OTCS) is a rare malformation syndrome with the following features: synostosis of metopic suture, craniofacial abnormalities, severe mental retardation and a multitude of pathological findings affecting almost every organ system. OTCS is associated with a high mortality rate. Case presentation: We describe the case of a Caucasian male baby who died at five months of age during surgical correction of the craniofacial anomaly. Conclusion: As previously reported, OTCS may have an increased mortality rate during craniofacial surgery. Careful evaluation of surgery risk-be nefit ratio is warranted in such patients. Introduction Opitz trigonocephaly C sy ndr ome (OTCS) is a rare and heterogeneous genetic disorder characterized by synos- tosis of metopic suture, dysmorphic facial features, vari- able mental retardation and other conge nital somatic and cerebral anomalies. Morbidity and mortality are very high. F ewer than 60 cases have been reported in the literature, mostly as single case reports or small ser- ies. We describe a white male baby who died at five months of age during surgery performed to correct the craniofacial anomaly. Case Presentation Our patient was a Caucasian baby, born to nonconsan- guineous parents at 39 weeks of gestational age. This was the first pregnancy of a 30-year-old mother with a bicornuate uterus. Pregnancy was complicated by early intrauterine growth retardation; antenatal ultrasound assessment was otherwise reported as normal. Labor and delivery were spontaneous. The Apgar score was 9 and 10, respectively at one and five minutes. Birth weight was 2470 g (< 3rd percentile, small for gestational age), length was 46.7 cm (3 rd to 10th percen- tile), head circumference 33.1 cm (10th percentile). At birth there was a marked trigonocephaly and other dysmorphic craniofacial features: micro gnathia, upslant- ing eyelids, hypotelorism, depressed nasal bridge, low set ears. Cardiac and renal ultrasounds were normal. Com- puted tomography confirmed the early closure of meto- picsuture(Figure1).Initiallythebabywasfedby nasogastric tube. At discharge after one week, he was fed completely by bottle. At 40 wks post-conceptional age brain MRI showed a small area of hyper-intensity under the posterior horn of the left ventricle (interpreted as calcification of a peri- ventricular hemorrhage) and a diffused alteration of white periventricular matter (Figure 2). An auditory brain stem response (ABR) test per- formed at 44 weeks revealed an absent pattern on the left ear. Clinical evaluation during the first four months of life did not show an evident psychomotor delay; however fidgety activity seemed absent. Chromosome analysis showed a normal 46 XY karyo- type. We also performed single-nucleotide polymorph- ism (SNP) array without any significant finding. The baby died unexpectedly at five months of age during surgery performed to correct the craniofacial anomaly. * Correspondence: ltravan@yahoo.it 1 Neonatal Intensive Care Unit, Institute for Maternal and Child Health Burlo Garofolo, Via dell’Istria 65/1, 34100, Trieste, Italy Full list of author information is available at the end of the article Travan et al. Journal of Medical Case Reports 2011, 5:222 http://www.jmedicalcasereports.com/content/5/1/222 JOURNAL OF MEDICAL CASE REPORTS © 2011 Travan et al; lic ense e BioMed Central Ltd. This is an Open Access article distributed under the te rms of the Creative Commons Attribution License (http://creativecommons.or g/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Autopsy did not add anything Clinical and epidemiological introduction Sudden infant death syndrome (SIDS) is the leading cause of postneonatal infant death, and represents the third leading cause of infant mortality overall in the USA [1]. As defined by Willinger et al. in 1991 [2], SIDS is described as the sudden death of an infant under 1 year of age which remains unexplained after a thorough case investigation, including performance of a complete autopsy, examination of the death scene, and review of clinical history. SIDS pathogenesis has been understood through a ‘triple risk hypothesis’. is argues that SIDS results from a convergence of three overlapping risk factors: (1) a vulnerable infant, (2) a critical development period, and (3) an exogenous stressor(s) [3]. An infant will only succumb to SIDS if and when all three over- lapping factors exist and converge. us, the inherent vulnerability of an infant will lie dormant until a crucial developmental period when the infant is then presented with the exogenous stressor. Nearly two decades ago, the 1994 ‘Back to Sleep’ campaign from the National Institute of Child Health and Human Development in the USA targeted such exogenous stressors as prone sleep, and reduced SIDS rates by more than 50% from 1.2 per 1,000 live births in 1992 to 0.55 per 1,000 live births in 2006, similar to reductions seen in Canada and many other countries [4,5]. However, despite these efforts, over 2,200 infants died of SIDS in 2004, and it appears that the recently witnessed reductions in deaths are diminishing [4]. Today, SIDS remains one of the leading causes of death for infants between 1 month and 1 year in developed countries [6], and current data suggest that approximately 60% to 80% of deaths under the age of 1 year remain autopsy negative [7,8]. Among developed countries, SIDS rates vary widely [6], and ethnic-specific disparities in rates have been noted. For example, SIDS rates are approximately twice as high among infants born to African American or American Indian mothers as compared with Caucasian mothers in the USA [5], and increases in SIDS risk are also seen for the Maoris in New Zealand, Aboriginal Australians [6], and those of mixed ancestry in Cape Town, South Africa [9]. In part, these data suggest that there may be genetic determinants of the ‘vulnerable infant,’ and many studies have examined the genetic makeup of SIDS cases. e first such report of a ‘genetic autopsy’ was published by Weinberg and Purdy in Nature in 1970 [10]. ey performed karyotype analysis on 17 SIDS cases, with 10 out of 11 available karyotypes declared abnormal compared with none in the living control group, suggesting a potential genetic link. Monumental technological Abstract Sudden infant death syndrome (SIDS) is a major contributor to postneonatal infant death, and is the third leading cause of infant mortality in the USA. While public health eorts have reduced these deaths in recent years, the pathogenesis of SIDS remains unclear. Epidemiological data on SIDS-related deaths have suggested genetic factors, and many studies have attempted to identify SIDS-associated genes. This has resulted in a large body of literature implicating various genes and their encoded proteins and signaling pathways in numerous cohorts of various sizes and ethnicities. This review has undertaken a systematic evaluation of these studies, identifying the pathways that have been implicated in these studies, including central nervous system pathways, cardiac channelopathies, immune dysfunction, metabolism/ energy pathways, and nicotine response. This review also explores how new genomic techniques will aid in advancing our knowledge of the genomic risk factors associated with SIDS, including SNPs and copy number variation. Last, this review explores how the current information can be applied to aid in our assessment of the at risk infant population. © 2010 BioMed Central Ltd Genomic risk Vietnamese - Number 46 January 2014 Hội Chứng Đột Tử Ở Trẻ Thơ Sudden Infant Death Syndrome (SIDS) Hội Chứng Đột Tử Ở Trẻ Thơ là gì? Hội Chứng Đột Tử Ở Trẻ Thơ (SIDS) xảy ra khi một em bé chết đột ngột trong lúc đang ngủ. SIDS thường xảy ra nhất ở các em bé từ 2 đến 4 tháng tuổi, và cái chết vẫn không giải thích được dù đã khám nghiệm trọn vẹn tử thi. Các nguyên nhân nào gây nên SIDS? Nguyên nhân của SIDS thì chưa rõ nhưng có những phương pháp rõ ràng cho ngủ an toàn được biết làm giảm nguy cơ đột tử ở trẻ thơ. Một số em bé, như các em sinh non và những em có số cân thấp khi mới sinh có nhiều rủi ro bị SIDS hơn những em khác. Tôi có thể làm gì để giảm thiểu rủi ro bị SIDS? Đặt con của quý vị nằm ngửa mỗi khi ngủ (ban đêm và khi ngủ các giấc ngắn ban ngày). Các em bé nằm ngửa để ngủ có ít rủi ro bị SIDS hơn những em bé nằm sấp hoặc nằm nghiêng một bên để ngủ. Các em bé khỏe mạnh và các trẻ sơ sinh không bị ngạt thở hoặc có các vấn đề khác về ngủ khi nằm ngửa. Khi con của quý vị có thể tự mình lăn qua để nằm sấp, thường từ lúc 5 đến 7 tháng tuổi thì không cần phải tiếp tục đặt các em nằm ngửa trở lại khi chúng trở mình trong giấc ngủ. Khi một em bé đang thức, em cần có một số thời gian tập ‘nằm sấp’. Các em bé nên được cho nằm sấp khi có sự hiện diện của những người chăm sóc trẻ và các em được coi chừng. Thời gian nằm sấp giúp cho các bắp thịt ở cổ và vai em bé được mạnh và ngừa các chỗ tạm thời bị phẳng ở phía sau đầu của em bé. Đặt con quý vị nằm trên một mặt phẳng cứng hoàn toàn không có các vật gây nguy hiểm. Hãy dùng giường dành cho em bé, nôi, hoặc xe đẩy có mui, có nệm cứng, khăn trải giường vừa khít và không để các miếng đệm thành giường, gối, mền nặng hoặc các đồ chơi trong đó. Hãy chắc chắn giường em bé, nôi hoặc xe đẩy có mui hội đủ các điều quy định về an toàn của Canada. Để biết thêm chi tiết về các quy định an toàn của Canada và để kiểm tra các sản phẩm bị gọi trả trở lại, hãy viếng trang mạng về An Toàn Sản Phẩm Cho Người Tiêu Thụ của Bộ Y Tế Canada tại www.hc-sc.gc.ca/cps-spc/index-eng.php . Để biết thêm thông tin về an toàn giường em bé, xin xem HealthLinkBC File #107 Ngủ An Toàn cho Trẻ Em. Hoàn toàn không hút thuốc khi mang thai và cho con quý vị có một môi trường hoàn toàn không có khói thuốc. Một em bé tiếp xúc với khói thuốc do người khác hút, hoặc mẹ của em đã hút thuốc trước khi và sau khi sanh, có nhiều rủi ro bị SIDS hơn. Đừng để những người khác hút thuốc gần nơi con quý vị, chẳng hạn như những người trong gia đình, bạn bè hoặc những người giữ trẻ. Hãy hỏi chuyên viên chăm sóc sức khỏe của quý vị nếu quý vị hoặc người bạn đời chung sống cần sự giúp đỡ để bỏ thuốc. Quý vị cũng có thể gọi đường dây giúp đỡ miễn phí QuitNow (Bỏ Ngay Bây Giờ) tại B.C. bằng cách gọi số 8-1-1 hay viếng mạng www.quitnow.ca . Ngủ chung phòng với con quý vị. Ngủ chung phòng giúp bảo vệ con quý vị chống lại SIDS, và đó là cách ngủ chung an toàn hơn là ngủ chung một giường. Trong 6 tháng đầu tiên, cho con quý vị ngủ chung phòng nhưng nằm riêng. Ngủ chung giường là điều không nên làm vì nó có thể đưa đến sự tử vong vì tai nạn và gia tăng rủi ro bị SIDS. Để biết thêm thông tin về các rủi ro của việc ngủ chung giường, xin xem HealthLinkBC File #107 Ngủ An Toàn cho Trẻ Em. Cho con quý vị bú sữa mẹ. Cho bú sữa mẹ giúp bảo vệ con quý vị chống lại SIDS. Bú sữa mẹ cũng giúp bảo vệ con quý vị tránh nhiều loại bệnh ở tuổi thơ. Sữa mẹ có tất cả các dưỡng chất con quý vị cần trong 6 tháng đầu tiên. Muốn biết Crib Death – Sudden Infant Death Syndrome (SIDS) Sudden Infant and Perinatal Unexplained Death: The Pathologist’s Viewpoint Second Edition Giulia Ottaviani Crib Death - Sudden Infant Death Syndrome (SIDS) Giulia Ottaviani Crib Death - Sudden Infant Death Syndrome (SIDS) Sudden Infant and Perinatal Unexplained Death: The Pathologist's Viewpoint Second Edition Giulia Ottaviani, MD, PhD Università degli Studi di Milano Milano Italy The University of Texas Health Science Center at Houston Houston, TX USA ISBN 978-3-319-08346-9 ISBN 978-3-319-08347-6 DOI 10.1007/978-3-319-08347-6 Springer Cham Heidelberg Dordrecht London New York (eBook) Library of Congress Control Number: 2014946575 © Springer International Publishing AG 2014 This work is subject to copyright All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed Exempted from this legal reservation are brief excerpts in connection with reviews or scholarly analysis or material supplied specifically for the purpose of being entered and executed on a computer system, for exclusive use by the purchaser of the work Duplication of this publication or parts thereof is permitted only under the provisions of the Copyright Law of the Publisher's location, in its current version, and permission for use must always be obtained from Springer Permissions for use may be obtained through RightsLink at the Copyright Clearance Center Violations are liable to prosecution under the respective Copyright Law The use of general descriptive names, registered names, trademarks, service marks, etc in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use While the advice and information in this book are believed to be true and accurate at the date of publication, neither the authors nor the editors nor the publisher can accept any legal responsibility for any errors or omissions that may be made The publisher makes no warranty, express or implied, with respect to the material contained herein Printed on acid-free paper Springer is part of Springer Science+Business Media (www.springer.com) A voice is heard in Ramah, lamentation and bitter weeping Rachel is weeping for her children and refuses to be comforted for her children are no more (Jeremiah 31:15) [1] To the memory of my beloved mother, Angela, my first inspiration, and to all parents whose lives are touched by the tragedy of a child’s illness or loss Reference Holy Bible: New revised standard version catholic edition (NRSV-CE), Catholic Biblical Association (1989) Bible Gateway http://www.biblegateway.com/ Accessed July 26, 2014 Foreword to the Second Edition The second edition of Dr Giulia Ottaviani’s monograph on crib death comes seven years after the first edition of this important work Some key features of the second edition are reflected in the title and subtitle The focus has been expanded based on convincing evidence for a continuum involving sudden infant death syndrome (SIDS), sudden perinatal unexpected death (SPUD), and sudden intrauterine death (SIUD) Together these entities continue to constitute a major public health problem with emotionally charged and tragic overtones for the involved parents SIDS affects one infant in every 1,700–2,000 live births, and represents the most frequent form of demise within the first year of life SIUD or unexplained stillbirth happens up to ten times more frequently than SIDS It continues to occur in about half of perinatal deaths in spite of advances in maternal and fetal care The other key feature of ...Definition • Sudden infant death syndrome (SIDS) is the unexplained death, usually during sleep, of a seemingly healthy baby Definition • Most SIDS deaths occur in children between... children between months and months of age Sudden infant death syndrome rarely occurs before month of age or after months Causes • Brain and nerve characteristics: Infants who die of SIDS may have brainstems... immunizations don't play a role in sudden infant death syndrome Risk factors • Male Boy babies are more likely to die of SIDS • Between month and months of age Infants are most vulnerable during