Journal articles: 'Sudden infant death syndrome – Etiology; Sudden infant death syndrome – Pathogenesis'

1

Pisaniak, Paulina, Dominika Piękoś, Katarzyna Bąk, Patryk Stokłosa, and Dorota Ozga. "The battle with uneven opponent – Sudden Infant Death Syndrome." Pielegniarstwo XXI wieku / Nursing in the 21st Century 18, no. 2 (June 1, 2019): 132–35. http://dx.doi.org/10.2478/pielxxiw-2019-0013.

Full text

Abstract:

AbstractSIDS is one of the biggest problems of modern medicine. In the diagnosis of SIDS, we take into account all possible diseases that may be the cause of death, as well as factors indicating an accident or murder. The etiology of SIDS is not yet known. There are several pathogenetic concepts, most of which refer to pathophysiological changes associated with nervous system hypoplasia. The most important risk factors include the effects of tobacco smoke, obstetric history, and incorrect sleep position. The role of risk factors in the pathogenesis of SIDS and their interdependence is still the subject of many studies. There are many theories developed on this subject, but none have been supported by scientific research and which is extremely difficult to carry out in this group of newborns. In most cases, medical help finds a newborn already dead, so it is difficult to say what is the main cause or marker of cot death. A considerable success in preventing the onset of sudden infant death syndrome turned out to be educational campaigns for parents - in order to follow up, an information leaflet was prepared with the basic recommendations in the prevention of SIDS. Among the parents of newborn children there are still many controversial opinions about risk factors in the onset of sudden infant death syndrome, the article contains and explains the meaning of individual activities that are considered to predispose to SIDS.

APA, Harvard, Vancouver, ISO, and other styles

2

ben-Aaron, M. "Sudden infant death syndrome: a cybernetic etiology." Medical Hypotheses 61, no. 5-6 (November 2003): 601–4. http://dx.doi.org/10.1016/s0306-9877(03)00242-1.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Byard, Roger W., and Henry F. Krous. "Sudden Infant Death Syndrome: Overview and Update." Pediatric and Developmental Pathology 6, no. 2 (March 2003): 112–27. http://dx.doi.org/10.1007/s10024-002-0205-8.

Full text

Abstract:

The past decade and a half has seen marked changes in the epidemiology of sudden infant death syndrome (SIDS). The avoidance of certain risk factors such as sleeping prone and cigarette smoke exposure has resulted in the death rate falling dramatically. Careful evaluation of environmental factors and endogenous characteristics has led to a greater understanding of the complexities of the syndrome. The development and implementation of death scene and autopsy protocols has led to standardization in approaches to unexpected infant deaths with increasing diagnoses of accidental asphyxia. Despite these advances, there is still confusion surrounding the diagnosis, with deaths being attributed to SIDS in many communities and countries where death scene investigations and autopsies have not been conducted. The following review provides a brief overview of the historical background, epidemiology, pathology, and pathogenesis of SIDS. Contentious issues concerning the diagnosis and current problems are discussed. Despite calls to abandon the designation, SIDS remains a viable term for infants who die in their sleep with no evidence of accident, inflicted injury, or organic disease after a full investigation has been conducted according to standard guidelines.

APA, Harvard, Vancouver, ISO, and other styles

4

Perrone, Serafina, Chiara Lembo, Sabrina Moretti, Giovanni Prezioso, Giuseppe Buonocore, Giorgia Toscani, Francesca Marinelli, Francesco Nonnis-Marzano, and Susanna Esposito. "Sudden Infant Death Syndrome: Beyond Risk Factors." Life 11, no. 3 (February 26, 2021): 184. http://dx.doi.org/10.3390/life11030184.

Full text

Abstract:

Sudden infant death syndrome (SIDS) is defined as “the sudden death of an infant under 1 year of age which remains unexplained after thorough investigation including a complete autopsy, death scene investigation, and detailed clinical and pathological review”. A significant decrease of SIDS deaths occurred in the last decades in most countries after the beginning of national campaigns, mainly as a consequence of the implementation of risk reduction action mostly concentrating on the improvement of sleep conditions. Nevertheless, infant mortality from SIDS still remains unacceptably high. There is an urgent need to get insight into previously unexplored aspects of the brain system with a special focus on high-risk groups. SIDS pathogenesis is associated with a multifactorial condition that comprehends genetic, environmental and sociocultural factors. Effective prevention of SIDS requires multiple interventions from different fields. Developing brain susceptibility, intrinsic vulnerability and early identification of infants with high risk of SIDS represents a challenge. Progress in SIDS research appears to be fundamental to the ultimate aim of eradicating SIDS deaths. A complex model that combines different risk factor data from biomarkers and omic analysis may represent a tool to identify a SIDS risk profile in newborn settings. If high risk is detected, the infant may be referred for further investigations and follow ups. This review aims to illustrate the most recent discoveries from different fields, analyzing the neuroanatomical, genetic, metabolic, proteomic, environmental and sociocultural aspects related to SIDS.

APA, Harvard, Vancouver, ISO, and other styles

5

Leiter, J. C., and Ines Böhm. "Mechanisms of pathogenesis in the Sudden Infant Death Syndrome." Respiratory Physiology & Neurobiology 159, no. 2 (November 2007): 127–38. http://dx.doi.org/10.1016/j.resp.2007.05.014.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Glinge, Charlotte, Sára Rossetti, Louise Bruun Oestergaard, Niels Kjær Stampe, Thomas Hadberg Lynge, Regitze Skals, Bo Gregers Winkel, et al. "Risk of Sudden Infant Death Syndrome Among Siblings of Children Who Died of Sudden Infant Death Syndrome in Denmark." JAMA Network Open 6, no. 1 (January 25, 2023): e2252724. http://dx.doi.org/10.1001/jamanetworkopen.2022.52724.

Full text

Abstract:

ImportanceSudden infant death syndrome (SIDS) remains a leading cause of death during the first year of life. The etiology of SIDS is complex and remains largely unknown.ObjectiveTo evaluate whether siblings of children who died of SIDS have a higher risk of SIDS compared with the general pediatric population.Design, Setting, and ParticipantsThis register-based cohort study used Danish nationwide registers. Participants were all infants (&lt;1 year) in Denmark between January 1, 1978, and December 31, 2016, including siblings of children who died of SIDS. Siblings were followed up from the index cases’ date of SIDS, date of birth, or immigration, whichever came first, and until age 1 year, emigration, developing SIDS, death, or study end. The median (IQR) follow-up was 1 (1-1) year. Data analysis was conducted from January 2017 to October 2022.Main Outcomes and MeasuresStandardized incidence ratios (SIRs) of SIDS were calculated with Poisson regression models relative to the general population.ResultsIn a population of 2 666 834 consecutive births (1 395 199 [52%] male), 1540 infants died of SIDS (median [IQR] age at SIDS, 3 [2-4] months) during a 39-year study period. A total of 2384 younger siblings (cases) to index cases (first sibling with SIDS) were identified. A higher rate of SIDS was observed among siblings compared with the general population, with SIRs of 4.27 (95% CI, 2.13-8.53) after adjustment for sex, age, and calendar year and of 3.50 (95% CI, 1.75-7.01) after further adjustment for mother’s age (&lt;29 years vs ≥29 years) and education (high school vs after high school).Conclusions and RelevanceIn this nationwide study, having a sibling who died of SIDS was associated with a 4-fold higher risk of SIDS compared with the general population. Shared genetic and/or environmental factors may contribute to the observed clustering of SIDS. The family history of SIDS should be considered when assessing SIDS risk in clinical settings. A multidisciplinary genetic evaluation of families with SIDS could provide additional evidence.

APA, Harvard, Vancouver, ISO, and other styles

7

Kaler, Jasndeep, Azhar Hussain, and Stanley Lee. "Manifestation and Pathogenesis of Sudden Infant Death Syndrome: A Review." Critical Reviews in Eukaryotic Gene Expression 30, no. 2 (2020): 111–20. http://dx.doi.org/10.1615/critreveukaryotgeneexpr.2020033009.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Wilders, Ronald. "Cardiac Ion Channelopathies and the Sudden Infant Death Syndrome." ISRN Cardiology 2012 (December 5, 2012): 1–28. http://dx.doi.org/10.5402/2012/846171.

Full text

Abstract:

The sudden infant death syndrome (SIDS) causes the sudden death of an apparently healthy infant, which remains unexplained despite a thorough investigation, including the performance of a complete autopsy. The triple risk model for the pathogenesis of SIDS points to the coincidence of a vulnerable infant, a critical developmental period, and an exogenous stressor. Primary electrical diseases of the heart, which may cause lethal arrhythmias as a result of dysfunctioning cardiac ion channels (“cardiac ion channelopathies”) and are not detectable during a standard postmortem examination, may create the vulnerable infant and thus contribute to SIDS. Evidence comes from clinical correlations between the long QT syndrome and SIDS as well as genetic analyses in cohorts of SIDS victims (“molecular autopsy”), which have revealed a large number of mutations in ion channel-related genes linked to inheritable arrhythmogenic syndromes, in particular the long QT syndrome, the short QT syndrome, the Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia. Combining data from population-based cohort studies, it can be concluded that at least one out of five SIDS victims carries a mutation in a cardiac ion channel-related gene and that the majority of these mutations are of a known malignant phenotype.

APA, Harvard, Vancouver, ISO, and other styles

9

Meny, Robert G., John L. Carroll, Mary Terese Carbone, and Dorothy H. Kelly. "Cardiorespiratory Recordings From Infants Dying Suddenly And Unexpectedly at Home." Pediatrics 93, no. 1 (January 1, 1994): 44–49. http://dx.doi.org/10.1542/peds.93.1.44.

Full text

Abstract:

Objective. Little is known about the mechanism of death during sudden infant death. To study the mechanism, we obtained data on six infants who died while on a memory-equipped cardiorespiratory monitor. Methods. Waveforms of respiration and heart rate trend were available for five infants; an alarm log only was available for the sixth. These printouts were reviewed with attention to mechanism and time to death. Results. All infants were born prematurely; autopsies reported the cause of death as sudden infant death syndrome in three cases and bronchopulmonary dysplasia in the others. Bradycardia, which played a more prominent role than central apnea, was preceded by tachycardia in two deaths. Resuscitation occurred within 1 minute in four cases; no response to alarms occurred in the other two cases, apparently because the parents were desensitized by prior meaningless alarms. Five patients died within 20 minutes, whereas one death due to sudden infant death syndrome was prolonged. Conclusion. Bradycardia is an important feature in all six of these infant deaths. Although its etiology is unknown, hypoxemia or obstructive apnea may precede bradycardia. Home monitors equipped to detect these possible antecedents will yield further insight into sudden infant death.

APA, Harvard, Vancouver, ISO, and other styles

10

Ponsonby, A. L., T. Dwyer, and M. E. Jones. "Sudden infant death syndrome: seasonality and a biphasic model of pathogenesis." Journal of Epidemiology & Community Health 46, no. 1 (February 1, 1992): 33–37. http://dx.doi.org/10.1136/jech.46.1.33.

Full text

APA, Harvard, Vancouver, ISO, and other styles

11

Becroft, David M. O., John M. D. Thompson, and Edwin A. Mitchell. "Epidemiology of Intrathoracic Petechial Hemorrhages in Sudden Infant Death Syndrome." Pediatric and Developmental Pathology 1, no. 3 (May 1998): 200–209. http://dx.doi.org/10.1007/s100249900027.

Full text

Abstract:

The possible effects of a wide range of sociodemographic and environmental factors on the incidence and distribution of petechiae were investigated in 485 sudden infant death syndrome (SIDS) cases from the New Zealand Cot Death Study. The number (nil, few, many) of macroscopic petechial hemorrhages in the visceral pleura, capsule of thymus, and epicardium was recorded in 458 of 474 autopsied SIDS cases. Other information was obtained from parental interview and obstetric records. Univariate analysis showed highly significant relationships ( P ≤ 0.005) between the frequency of petechiae at one or more sites and socioeconomic status, parity, breast feeding, age at death, time of death, sleep position, and head covering at death and lesser but significant relationships ( P ≤ 0.05) with Maori ethnicity, birth weight, gestation, pacifier use, and bed sharing. After multivariate analysis, significant associations remained between increased frequencies of thymic petechiae and parity (P = 0.0001), age at death (P = 0.0003), Maori ethnicity (P = 0.0019), pacifier use (P = 0.0001), and head covering at death (P = 0.0032); between increased frequencies of epicardial petechiae and head covering at death (P = 0.008) and an estimated time of death between 00:00 and 05:59 h ( P = 0.056); and between increased frequencies of pleural petechiae and maternal smoking ( P = 0.058) and parity ( P = 0.022). There was a decreased frequency of pleural petechiae in infants placed prone for their final sleep ( P = 0.058). The distribution and frequency of petechiae are affected by environmental factors, including known risk factors for SIDS, but these factors occur inconsistently across the three sites. The findings imply differences in the pathogenesis at each site but do not provide consistent support for previous theories of causation of petechiae.

APA, Harvard, Vancouver, ISO, and other styles

12

Goldwater, Paul N. "Intrathoracic Petechial Hemorrhages in Sudden Infant Death Syndrome and other Infant Deaths: Time for Re-Examination?" Pediatric and Developmental Pathology 11, no. 6 (November 2008): 450–55. http://dx.doi.org/10.2350/08-01-0404.1.

Full text

Abstract:

The objective of this study was to provide a predictive tool to assist forensic and pediatric pathologists in the diagnosis of sudden unexpected infant death and to discuss the pathogenesis of intrathoracic petechial hemorrhages through a retrospective autopsy report review of 174 sudden infant death syndrome (SIDS) cases (2004 definition) and 67 age-matched comparison deaths. The setting was a qualitative assessment (presence or absence) of macroscopic intrathoracic petechiae in SIDS and age-matched comparison of sudden unexpected deaths that occurred in the late 1980s and early 1990s. Sensitivity, specificity, and positive and negative predictive values for thymic, pleural, and epicardial petechial hemorrhages were developed. Results showed 89.5%, 80%, and 79.9% SIDS (<12 months of age) had thymic, pleural, and epicardial petechiae, respectively, compared with 47.6%, 47.5% and 43.6% in non-SIDS deaths, respectively. Respective odds ratios were: 9.4 (4.5 to 19.9), 4.6 (2.3 to 9.1), 5.3 (2.6 to 10.8). When all 3 intrathoracic organ sites contain macroscopic petechiae, this is 84.9% predictive of SIDS; when all 3 sites have no detectable petechiae this is 93.1% predictive of a non-SIDS diagnosis. Thus, we conclude that careful assessment of intrathoracic petechiae at autopsy is likely to be diagnostically useful in the assessment of sudden unexplained infant death.

APA, Harvard, Vancouver, ISO, and other styles

13

Becker, L. E., and W. Zhang. "Vagal Nerve Complex in Normal Development and Sudden Infant Death Syndrome." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 23, no. 1 (February 1996): 24–33. http://dx.doi.org/10.1017/s0317167100039147.

Full text

Abstract:

ABSTRACT:Background:Although the pathogenesis of sudden infant death syndrome (SIDS) is not understood, one of the major hypotheses is that a subtle defect in respiratory circuitry is an important underlying factor. The vagus nerve is a critical component of respiratory control, but its neuroanatomic complexity has limited its investigation in human disease.Methods:Correlating developmental studies on different parts of the vagus nerve allows a more comprehensive assessment of its maturation process. Comparison of the normal developing vagus nerve with nerves examined in SIDS patients suggests alterations in the nucleus tractus solitarius and dorsal vagal nucleus as well as in the peripheral vagus nerve.Results and Conclusions:The persistence of dendritic spines and lack of appropriate axonal growth implies delays in vagal maturation. Since nodose ganglia can be examined in vitro from autopsy material, perturbation to this system can be explored to evaluate further the mechanism involved in terminal vagal maturation. Although the reason for the delayed vagal maturation in SIDS is not apparent, the presence of astrogliosis in the region of the vagal nuclei is consistent with an exposure to hypoxic-ischemic events some time before death.

APA, Harvard, Vancouver, ISO, and other styles

14

Johannsen, Emma B., Linda B. Baughn, Neeraj Sharma, Nicolina Zjacic, Mehdi Pirooznia, and Eran Elhaik. "The Genetics of Sudden Infant Death Syndrome—Towards a Gene Reference Resource." Genes 12, no. 2 (February 2, 2021): 216. http://dx.doi.org/10.3390/genes12020216.

Full text

Abstract:

Sudden infant death syndrome (SIDS) is the unexpected death of an infant under one year of age that remains unexplained after a thorough investigation. Despite SIDS remaining a diagnosis of exclusion with an unexplained etiology, it is widely accepted that SIDS can be caused by environmental and/or biological factors, with multiple underlying candidate genes. However, the lack of biomarkers raises questions as to why genetic studies on SIDS to date are unable to provide a clearer understanding of the disease etiology. We sought to improve the identification of SIDS-associated genes by reviewing the SIDS genetic literature and objectively categorizing and scoring the reported genes based on the strength of evidence (from C1 (high) to C5 (low)). This was followed by analyses of function, associations between genes, the enrichment of gene ontology (GO) terms, and pathways and gender difference in tissue gene expression. We constructed a curated database for SIDS gene candidates consisting of 109 genes, 14 of which received a category 4 (C4) and 95 genes received the lowest category of C5. That none of the genes was classified into the higher categories indicates the low level of supporting evidence. We found that genes of both scoring categories show distinct networks and are highly diverse in function and involved in many GO terms and pathways, in agreement with the perception of SIDS as a heterogeneous syndrome. Genes of both scoring categories are part of the cardiac system, muscle, and ion channels, whereas immune-related functions showed enrichment for C4 genes. A limited association was found with neural development. Overall, inconsistent reports and missing metadata contribute to the ambiguity of genetic studies. Considering those parameters could help improve the identification of at-risk SIDS genes. However, the field is still far from offering a full-pledged genetic test to identify at-risk infants and is still hampered with methodological challenges and misunderstandings of the vulnerabilities of vital biological mechanisms.

APA, Harvard, Vancouver, ISO, and other styles

15

Schechtman, Vicki L., Ronald M. Harper, Adrian J. Wilson, and David P. Southall. "Sleep Apnea in Infants Who Succumb to The Sudden Infant Death Syndrome." Pediatrics 87, no. 6 (June 1, 1991): 841–46. http://dx.doi.org/10.1542/peds.87.6.841.

Full text

Abstract:

Previous studies have shown the frequency of respiratory pauses to be altered in groups of infants at risk for the sudden infant death syndrome (SIDS). In this study, we assess the frequency of apneic pauses during quiet sleep and rapid eye movement sleep in control infants and infants who subsequently died of SIDS. Sleep states were identified in 12-hour physiological recordings of SIDS victims and matched control infants, and the number of respiratory pauses from 4 to 30 seconds in duration was computed for quiet sleep and rapid eye movement sleep. SIDS victims 40 to 65 days of age showed significantly fewer apneic pauses than did age-matched control infants across the two sleep states. Fewer short respiratory pauses accounted for most of the reduction in number of apneic events in the SIDS victims during both sleep states. During the first month of life, SIDS victims did not differ significantly from control neonates on this measure. The finding that this respiratory difference exists during the second month of life, just before the period of maximal risk for SIDS, but not earlier, may have implications for the etiology of SIDS deaths.

APA, Harvard, Vancouver, ISO, and other styles

16

Courts, Cornelius, Melanie Grabmüller, and Burkhard Madea. "Monoamine Oxidase A Gene Polymorphism and the Pathogenesis of Sudden Infant Death Syndrome." Journal of Pediatrics 163, no. 1 (July 2013): 89–93. http://dx.doi.org/10.1016/j.jpeds.2012.12.072.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Bettelheim, K. A., R. K. J. Luke, N. Johnston, J. L. Pearce, and P. N. Goldwater. "A Possible Murine Model for Investigation of Pathogenesis of Sudden Infant Death Syndrome." Current Microbiology 64, no. 3 (December 17, 2011): 276–82. http://dx.doi.org/10.1007/s00284-011-0065-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

Kinney, Hannah C. "Neuropathology provides new insight in the pathogenesis of the sudden infant death syndrome." Acta Neuropathologica 117, no. 3 (February 10, 2009): 247–55. http://dx.doi.org/10.1007/s00401-009-0490-7.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

Denisova, Yu V., L. S. Aleksandrov, A. I. Ishchenko, A. P. Nikonov, E. E. Rudenko, M. N. Zholobova, M. V. Berishvili, et al. "Perinatal mortality of unspecified (unknown) etiology: problems and solutions." Voprosy ginekologii, akušerstva i perinatologii 21, no. 4 (2022): 99–115. http://dx.doi.org/10.20953/1726-1678-2022-4-99-115.

Full text

Abstract:

According to the World Health Organization, there are about 5.9 million annual perinatal deaths worldwide, the etiology of which, on average, remains unspecified in 15–50% of cases. This review presents an analysis of the existing classification systems for causes of perinatal mortality, estimates the current data on risk factors and possible pathophysiological mechanisms of sudden fetal and infant death, identifies several world health problems that prevent the reduction of stillbirth and neonatal mortality rates, and suggests the ways of their solution. Key words: perinatal mortality, stillbirth, sudden intrauterine death syndrome, brainstem, cardiac conduction system

APA, Harvard, Vancouver, ISO, and other styles

20

Dollfus, Catherine, Michael Patetta, Earl Siegel, and Alan W. Cross. "Infant Mortality: A Practical Approach to the Analysis of the Leading Causes of Death and Risk Factors." Pediatrics 86, no. 2 (August 1, 1990): 176–83. http://dx.doi.org/10.1542/peds.86.2.176.

Full text

Abstract:

The analysis of infant mortality data provides an opportunity for developing preventive strategies to improve this indicator of a population's health. All infant deaths in North Carolina during a 5-year period (1980 through 1984) were analyzed using the International Classification of Diseases, 9th revision (ICD-9), and a system for linked birth and death records that allows the analysis of birth certificate information on deaths. Causes of death were aggregated based on common etiology such as prematurity or obstetric-related conditions rather than the more traditional organ system taxonomy of the ICD-9 codes. Analyses were carried out separately for very low birth weight (≤1500 g), moderately low birth weight (1501 through 2500 g), and normal birth weight (>2500 g) babies. Maternal characteristics identified from the birth certificate were also compared with the different causes of death. Prematurity-related conditions accounted for 37.5% of all deaths, ranking far above the 17.4% for congenital anomalies and 12.9% for sudden infant death syndrome. For normal birth weight babies, sudden infant death syndrome ranked first, followed by congenital anomalies and nonperinatal infections. For the moderately low birth weight babies, congenital anomalies ranked first, with sudden infant death syndrome second and prematurity-related conditions third. For the very low birth weight babies, prematurity-related conditions accounted for nearly 70% of the deaths, with obstetric conditions and congenital anomalies ranking second and third, respectively. Maternal risk factors identified an overrepresentation of nonwhite, unmarried, and young teenage mothers and mothers with less than adequate prenatal care. This system for analyzing infant deaths provides an opportunity to devise preventive strategies by identifying common underlying conditions, such as prematurity, that account for a high proportion of deaths.

APA, Harvard, Vancouver, ISO, and other styles

21

Matschke, Jakob, Jan-Peter Sperhake, Nadine Wilke, Klaus Püschel, and Markus Glatzel. "Cerebellar heterotopia of infancy in sudden infant death syndrome: an observational neuropathological study of four cases." International Journal of Legal Medicine 134, no. 6 (May 21, 2020): 2143–47. http://dx.doi.org/10.1007/s00414-020-02316-x.

Full text

Abstract:

Abstract Sudden infant death syndrome (SIDS) is the sudden unexpected death of an infant < 1 year of age that remains unexplained after comprehensive workup including complete autopsy and investigation of the circumstances of death. The triple risk hypothesis posits that SIDS results as a combination of both intrinsic and extrinsic factors on the background of a predisposing vulnerability. Neuropathological examination in the past has focussed mainly on the brainstem as the major player in respiratory control, where subtle findings have been linked to the chain of events leading to death in SIDS. The cerebellum has received less attention, probably due to an assumed negligible role in central cardiorespiratory control. We report four cases of SIDS in which neuropathological investigation revealed cerebellar heterotopia of infancy, a distinct malformation of the cerebellum, and discuss the potential impact of this condition on the aetiology and pathogenesis of SIDS.

APA, Harvard, Vancouver, ISO, and other styles

22

Roesdahl, Ingeborg, and Jørgen L. Thomsen. "2. Sudden Infant Death Syndrome and Lipoma: The Presence of Fat Tissue in the Spinal Canal." Medicine, Science and the Law 35, no. 4 (October 1995): 354–56. http://dx.doi.org/10.1177/002580249503500415.

Full text

Abstract:

An epidural lipoma in the spinal canal in a case of Sudden Infant Death Syndrome (SIDS) is described. Histologic sections from ten SIDS cases were compared with five controls. It is concluded that there are no indications that an increased amount of fat in the spinal canal plays a role in the pathogenesis of SIDS.

APA, Harvard, Vancouver, ISO, and other styles

23

Lavezzi, Anna Maria. "Altered Development of Mesencephalic Dopaminergic Neurons in SIDS: New Insights into Understanding Sudden Infant Death Pathogenesis." Biomedicines 9, no. 11 (October 26, 2021): 1534. http://dx.doi.org/10.3390/biomedicines9111534.

Full text

Abstract:

Sudden infant death syndrome (SIDS) is defined as the unexpected sudden death of an infant under 1 year of age that remains unexplained after a thorough case investigation. The SIDS pathogenesis is still unknown; however, abnormalities in brain centers that control breathing and arousal from sleep, including dramatic changes in neurotransmitter levels, have been supposed in these deaths. This is the first study focusing on mesencephalic dopaminergic neurons, so far extensively studied only in animals and human neurological diseases, in SIDS. Dopaminergic structures in midbrain sections of a large series of sudden infant deaths (36 SIDS and 26 controls) were identified using polyclonal rabbit antibodies against tyrosine hydroxylase, the rate-limiting enzyme in catecholamine biosynthesis, and the dopamine transporter, a membrane protein specifically expressed in dopaminergic cells. Dopamine-immunolabeled neurons were observed concentrated in two specific structures: the pars compacta of the substantia nigra and in the subnucleus medialis of the periaqueductal gray matter. Anatomical and functional degenerations of dopaminergic neurons in these regions were observed in most SIDS cases but never in controls. These results indicate that dopamine depletion, which is already known to be linked especially to Parkinson’s disease, is strongly involved even in SIDS pathogenesis.

APA, Harvard, Vancouver, ISO, and other styles

24

Blood-Siegfried, Jane, Margaret T. Bowers, and Marcia Lorimer. "Is Shock a Key Element in the Pathology of Sudden Infant Death Syndrome (SIDS)?" Biological Research For Nursing 11, no. 2 (December 28, 2008): 187–94. http://dx.doi.org/10.1177/1099800408324854.

Full text

Abstract:

In developed countries, sudden infant death syndrome (SIDS) is the most common cause of death for infants between 1 month and 1 year of age. The etiology of SIDS is likely to be multifactorial, and current paradigms often describe three overlapping elements of risk. Those elements are a critical developmental period, a vulnerable infant, and one or more exogenous stressors. In the triple-risk model, SIDS infants are described as having an underlying vulnerability in cardiorespiratory control in the central nervous system during a critical period when autonomic control is developing. This vulnerability might affect the response to exogenous stressors, including prone sleeping position, hypoxia, and increased carbon dioxide. In the common bacterial hypothesis and fatal triangle, the focus is on the stressors. In the first, a combination of common respiratory infections can cause SIDS in an infant during a developmentally vulnerable period. This theory also includes 3 factors of vulnerability: a genetic predisposition, a vulnerable developmental age, and infectious stressors. In the fatal triangle theory, infection, inflammation, and genetics each play a role in triggering a SIDS fatality. From our work in an animal model, we have found that rat pups die from a combination of infectious insults during a critical time of development. This is exacerbated by perinatal nicotine exposure, a condition shown to alter the autonomic response in exposed offspring. We are proposing that shock and cardiovascular collapse is a key element that links these theories.

APA, Harvard, Vancouver, ISO, and other styles

25

Cochran-Black, Diana L., Linda D. Cowan, and Barbara R. Neas. "The Relation Between Newborn Hemoglobin F Fractions and Risk Factors for Sudden Infant Death Syndrome." Archives of Pathology & Laboratory Medicine 125, no. 2 (February 1, 2001): 211–17. http://dx.doi.org/10.5858/2001-125-0211-trbnhf.

Full text

Abstract:

Abstract Objectives.—The aims of this study were to determine and compare fetal hemoglobin (HbF) fractions at birth in newborns exposed and not exposed to selected factors that have been reported to increase the risk of sudden infant death syndrome (SIDS). Previous studies have implicated HbF in the etiology of SIDS by finding higher fractions in infants dying from SIDS compared to age-matched control infants. Design.—We performed a cross-sectional study using high-performance liquid chromatography to measure HbF fractions in newborn cord blood samples. Exposure to selected risk factors for SIDS was assessed through review of medical records. Participants.—Six hundred thirty-three infants born at Via Christi Regional Medical Center–St Francis Campus, Wichita, Kan, from February 28 through August 5, 1997. Main Outcome Measure.—Hemoglobin F fractions at birth were compared in newborns exposed and not exposed to selected risk factors associated with increased incidence of SIDS. Results.—Mean HbF fractions were significantly higher in preterm newborns of mothers who smoked and in term newborns with intrauterine growth restriction, pregnancy weight gain less than or equal to 9 kg, and pregnancy complications associated with reduced placental blood flow. An elevated newborn HbF fraction, defined as 77% or greater, was significantly associated with maternal smoking, maternal anemia, intrauterine growth restriction, and pregnancy complications associated with reduced placental blood flow. Conclusion.—This study suggests a possible mechanism (HbF) by which previously identified factors may increase the risk of SIDS.

APA, Harvard, Vancouver, ISO, and other styles

26

Curran, Aidan K., Robert A. Darnall, James J. Filiano, Aihua Li, and Eugene E. Nattie. "Muscimol dialysis in the rostral ventral medulla reduced the CO2 response in awake and sleeping piglets." Journal of Applied Physiology 90, no. 3 (March 1, 2001): 971–80. http://dx.doi.org/10.1152/jappl.2001.90.3.971.

Full text

Abstract:

Some victims of sudden infant death syndrome have arcuate nucleus abnormalities. The arcuate nucleus may be homologous with ventral medullary structures in the cat known to be involved in the control of breathing and the response to systemic hypercapnia. We refer to putative arcuate homologues in the piglet collectively as the rostral ventral medulla (RVM). We inhibited the RVM in awake and sleeping, chronically instrumented piglets by microdialysis of the GABAA receptor agonist muscimol. Muscimol dialysis (10 and 40 mM) had no effect on eupnea but caused a significant reduction in the response to hypercapnia during both wakefulness (34.8 ± 8.7 and 30.7 ± 10.1%, respectively) and sleep (36.7 ± 6.7 and 49.5 ± 8.9%, respectively). The effect of muscimol on the CO2 response was entirely via a reduction in tidal volume and appeared to be greater during non-rapid-eye-movement sleep. We conclude that the piglet RVM contains neurons of importance in the response to systemic CO2 during both wakefulness and non-rapid-eye-movement sleep. We hypothesize that dysfunction of homologous regions in the human infant could lead to impaired ability to respond to hypercapnia, particularly during sleep, which could potentially be involved in the pathogenesis of sudden infant death syndrome.

APA, Harvard, Vancouver, ISO, and other styles

27

Shaw, W. "Possible role of lysolecithins and nonesterified fatty acids in the pathogenesis of Reye's syndrome, sudden infant death syndrome, acute pancreatitis, and diabetic ketoacidosis." Clinical Chemistry 31, no. 7 (July 1, 1985): 1109–15. http://dx.doi.org/10.1093/clinchem/31.7.1109.

Full text

Abstract:

Abstract In vitro denaturation and (or) alteration of protein function by detergents have been extensively documented. I suggest that similar biochemical and clinical features of Reye's syndrome, sudden infant death syndrome, acute pancreatitis, and diabetic ketoacidosis may be explained as sequelae of the toxic detergent effects of nonesterified fatty acids and lysolecithins. These diseases may be provoked by a drug-induced diminution of the detergent-buffering capacity of blood or tissue proteins; by excess detergents produced in vivo, consequent to lipase activity induced by viral infection or metabolic disease; or by some combination of these factors.

APA, Harvard, Vancouver, ISO, and other styles

28

Ivanov, Dmitry, Ekaterina Mironova, Victoria Polyakova, Inna Evsyukova, Michail Osetrov, Igor Kvetnoy, and Ruslan Nasyrov. "Sudden infant death syndrome: Melatonin, serotonin, and CD34 factor as possible diagnostic markers and prophylactic targets." PLOS ONE 16, no. 9 (September 10, 2021): e0256197. http://dx.doi.org/10.1371/journal.pone.0256197.

Full text

Abstract:

Sudden infant death syndrome (SIDS) is one of the primary causes of death of infants in the first year of life. According to the WHO’s data, the global infant mortality rate is 0.64–2 per 1,000 live-born children. Molecular and cellular aspects of SIDS development have not been identified so far. The purpose of this paper is to verify and analyze the expression of melatonin 1 and 2 receptors, serotonin (as a melatonin precursor), and CD34 molecules (as hematopoietic and endothelial markers of cardiovascular damage) in the medulla, heart, and aorta in infants who died from SIDS. An immunohistochemical method was used to investigate samples of medulla, heart, and aorta tissues of infants 3 to 9 months of age who died from SIDS. The control group included children who died from accidents. It has been shown that the expression of melatonin receptors as well as serotonin and CD34 angiogenesis markers in tissues of the medulla, heart, and aorta of infants who died from SIDS is statistically lower as compared with their expression in the same tissues in children who died from accidents. The obtained data help to clarify in detail the role of melatonin and such signaling molecules as serotonin and CD34 in SIDS pathogenesis, which can open new prospects for devising novel methods for predictive diagnosis of development and targeted prophylaxis of SIDS.

APA, Harvard, Vancouver, ISO, and other styles

29

Bulterys, Marc G., Sander Greenland, and Jess F. Kraus. "Chronic Fetal Hypoxia and Sudden Infant Death Syndrome: Interaction Between Maternal Smoking and Low Hematocrit During Pregnancy." Pediatrics 86, no. 4 (October 1, 1990): 535–40. http://dx.doi.org/10.1542/peds.86.4.535.

Full text

Abstract:

To investigate the hypothesis that chronic fetal hypoxia contributes to the etiology of sudden infant death syndrome (SIDS), a possible interaction between the effect of maternal cigarette smoking and low hematocrit during pregnancy on the risk of SIDS was studied using the US Collaborative Perinatal Project cohort. The 193 SIDS cases identified in the cohort were analyzed with 1930 controls randomly selected from infants who survived the first year of life. After adjustment for maternal age, infants born to mothers who smoked 10 or more cigarettes per day and who were anemic (hematocrit less than 30%) during pregnancy were at a much higher risk of SIDS than infants born to mothers who did not smoke and were not anemic (odds ratio = 4.0; 95% confidence limits, 2.1 and 7.4). Smoking 10 or more cigarettes per day vs none increased the risk of SIDS by 70% among women with hematocrit at or above 30% but increased risk threefold among women with hematocrit below 30%. After adjustment for more potential confounders in a logistic regression model, the effect of smoking on SIDS continued to increase with lower levels of hematocrit during pregnancy. Birth weight accounted for very little of these associations. Low hematocrit was not a risk factor for SIDS among nonsmokers but became an important predictor among heavy smokers. These findings are in agreement with the hypothesis that chronic fetal hypoxia may predispose to SIDS, possibly by impairing the normal development of the fetal central nervous system.

APA, Harvard, Vancouver, ISO, and other styles

30

Ottaviani, Giulia, and L. Maximilian Buja. "Update on congenital heart disease and sudden infant/perinatal death: from history to future trends." Journal of Clinical Pathology 70, no. 7 (April 27, 2017): 555–62. http://dx.doi.org/10.1136/jclinpath-2017-204326.

Full text

Abstract:

During the 20th century, expert pathologists contributed an in-depth characterisation of the anatomical pathology and associated pathophysiology of congenital heart disease (CHD). Starting in the 1970s, the reported CHD birth prevalence has been increasing, owing to advances in diagnostic methods. Over the years, surgical treatments have been associated with an enormous reduction of CHD mortality. Advances also have been made in understanding the developmental biology and molecular pathogenesis of CHD. In developed countries, sudden infant death syndrome (SIDS) is the most frequent form of death during the first year of life, with a death rate of 0.42 every 1000 births. Unexpected stillbirth has a six- to eightfold greater incidence than that of SIDS and remains unexplained in 40–80% of cases even after autopsy. Specific environmental risk factors, such as maternal smoking, air and water pollution, food contamination, pesticides, etc, can interact with the genetic constitution in complex ways, which may lead to polymorphisms and/or mutations of specific genes, such as polymorphisms in the serotonin transporter gene 5-HTT, the regulator of the synaptic serotonin concentration. Current directions of research in this area are reviewed.

APA, Harvard, Vancouver, ISO, and other styles

31

Zhou, Qiaoxia, Daoyin Gong, Yu Zhang, and Feijun Huang. "Association between monoamine oxidase A promoter polymorphism and the risk of sudden infant death syndrome: a meta-analysis." International Journal of Legal Medicine 135, no. 4 (February 1, 2021): 1179–90. http://dx.doi.org/10.1007/s00414-020-02496-6.

Full text

Abstract:

Abstract Introduction The etiology of sudden infant death syndrome (SIDS) remains an unsolved problem. The aim of this meta-analysis is to investigate the potential association between monoamine oxidase A (MAOA) promoter variable number tandem repeat (VNTR) polymorphism and SIDS risk. Methods A systematic review and meta-analysis were conducted on studies from accessible electronic databases. Each VNTR variant was examined in each gender independently by comparing with the pooled results of other alleles. Results A total of six independent case–control studies including 1022 SIDS cases and 1839 controls were enrolled in this meta-analysis. In both of the whole populations and Caucasian populations, male infants with the low-MAOA-expression alleles (2R+3R) were found to exhibit a statistically significant increased risk of SIDS, whereas those with a 4R allele exhibited a reduced risk of SIDS. Besides, an increased risk of SIDS was detected in male Caucasian infants with 2R or 3R alleles. However, none of the allele or genotype variants was associated with SIDS in female victims. Conclusion In male Caucasian infants, the low expression of MAOA promoter VNTR alleles (2R and 3R) is associated with an increased risk of SIDS, and the existence of the 4R allele could be regarded as a protective factor.

APA, Harvard, Vancouver, ISO, and other styles

32

Lavezzi, Anna M., Riffat Mehboob, Graziella Alfonsi, and Stefano Ferrero. "Substantia Nigra Abnormalities Provide New Insight on the Neural Mechanisms Underlying the Sleep-Arousal Phase Dysfunctions in Sudden Infant Death Syndrome." ASN Neuro 12 (January 2020): 175909142096269. http://dx.doi.org/10.1177/1759091420962695.

Full text

Abstract:

The purpose of this study was to research possible developmental alterations of the substantia nigra (SN) in sudden infant death syndrome (SIDS), a syndrome frequently attributed to arousal failure from sleep. Brain stems of 46 victims of sudden infant death, aged from 1 to about 7 months (4 to 30 postnatal weeks), were investigated. Twenty-six of these cases were diagnosed as SIDS, due to the lack of any pathological finding, while the remaining 20 cases in which the cause of death was determined at autopsy served as controls. Maternal smoking was reported in 77% of SIDS and 10% of controls. Histopathological examination of the SN was done on 5-µm-thick sections of caudal midbrain stained with both hematoxylin-eosin and Klüver-Barrera. Densitometry, immunohistochemistry and histochemistry were applied to highlight the neuronal concentration, the tyrosine hydroxylase (TH) expression, and the presence of neuromelanin (NM) in this structure. Hypoplasia of the pars compacta portion of the SN was observed in 69% of SIDS but never in controls; TH expression was significantly higher in controls than in SIDS; and NM was observed only in 4 infants of the control group but not in SIDS. A significant correlation was found between SIDS, hypoplasia/low neuronal density, low TH expression in the pars compacta, and maternal smoking. Because the SN pars compacta, being the major dopamine brain center, controls many functions, including the sleep-arousal phase, its alterations, especially concurrently with smoking exposure, may contribute to explain the pathogenesis of SIDS that occur in the great part of cases at awakening from sleep.

APA, Harvard, Vancouver, ISO, and other styles

33

Bright, Fiona M., Robert Vink, and Roger W. Byard. "The potential role of substance P in brainstem homeostatic control in the pathogenesis of sudden infant death syndrome (SIDS)." Neuropeptides 70 (August 2018): 1–8. http://dx.doi.org/10.1016/j.npep.2018.02.006.

Full text

APA, Harvard, Vancouver, ISO, and other styles

34

Paterson, David S. "Serotonin gene variants are unlikely to play a significant role in the pathogenesis of the sudden infant death syndrome." Respiratory Physiology & Neurobiology 189, no. 2 (November 2013): 301–14. http://dx.doi.org/10.1016/j.resp.2013.07.001.

Full text

APA, Harvard, Vancouver, ISO, and other styles

35

Wright, James R. "A Fresh Look at the History of SIDS." Academic Forensic Pathology 7, no. 2 (June 2017): 146–62. http://dx.doi.org/10.23907/2017.017.

Full text

Abstract:

Sudden infant death syndrome (SIDS) became a named entity in 1969 and the term has been used to certify sudden unexpected infant deaths meeting certain demographic, epidemiologic, and pathologic criteria. Since it is a diagnosis of exclusion, there is inherent imprecision, and this has led the National Association of Medical Examiners to recommend that these deaths now be classified as “undetermined.” This historical review article briefly analyzes anecdotal instances of SIDS described centuries ago as overlying, smothering, infanticide, and suffocation by bedclothes followed by a more detailed review of “thymic” causes (i.e., thymic asthma and status thymicolymphaticus) popular in the late 1800s and early 1900s. Before the 1950s, such cases were also often categorized as accidental mechanical suffocation. In the 1940s and 1950s, forensic studies on infants dying unexpectedly revealed a typical pattern of autopsy findings strongly suggestive of natural causation and, after 1969, cases meeting the appropriate criteria were usually categorized as SIDS, a term embraced by the public and by advocacy groups. Research conducted after the 1960s identified important risk factors and generated many theories related to pathogenesis, such as prolonged sleep apnea. The incidence of SIDS deaths decreased sharply in the early 1990s after implementing public awareness programs addressing risk factors such as prone sleeping position and exposure to smoking. Deletion of cases in which death scene investigation suggested asphyxiation and cases where molecular autopsies revealed metabolic diseases further decreased the incidence. This historical essay lays the foundation for debate on the future of the SIDS entity.

APA, Harvard, Vancouver, ISO, and other styles

36

Clayton, Ellen Wright. "The Complex Relationship of Genetics, Groups, and Health: What it Means for Public Health." Journal of Law, Medicine & Ethics 30, no. 2 (2002): 290–97. http://dx.doi.org/10.1111/j.1748-720x.2002.tb00395.x.

Full text

Abstract:

Genetics offers real opportunities for public health actors. Increased understanding of genetics will illuminate some of the factors that affect disease and, in many cases, will lead to more effective treatments. The recognition that phenylketonuria was caused by a metabolic defect that led to the accumulation of toxic levels of phenylalanine, an elevation that could largely be averted by adopting a low-phenylalanine diet, is an early example. Some cases of what was thought to be Sudden Infant Death Syndrome, a diagnosis used when no etiology is known, now appear to have been caused by metabolic defects in fatty acid oxidation and sodium channel defects. One of the tasks that has already been undertaken by the public health sector is to ensure that genomic information is incorporated into clinical care when the robusmess of findings and their clinical utility have been well defined.

APA, Harvard, Vancouver, ISO, and other styles

37

Klintschar, Michael. "The Association Between Polymorphisms in Serotonin-Related Genes and Pain Modulation Might Be of Importance for the Pathogenesis of Sudden Infant Death Syndrome." Journal of Pain 13, no. 5 (May 2012): 516. http://dx.doi.org/10.1016/j.jpain.2011.12.004.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

Curran, Aidan K., Daniel Peraza, Cheryl A. Elinsky, and J. C. Leiter. "Enhanced baroreflex-mediated inhibition of respiration after muscimol dialysis in the rostroventral medulla." Journal of Applied Physiology 92, no. 6 (June 1, 2002): 2554–64. http://dx.doi.org/10.1152/japplphysiol.00895.2001.

Full text

Abstract:

The rostral ventral medulla (RVM) may be important in the control of cardiorespiratory interactions. We hypothesized that inhibition of the RVM would enhance inhibition of breathing associated with transient blood pressure elevations. In 25 piglets 3–16 days of age, we studied the effect of acutely increasing blood pressure, by systemic infusion of phenylephrine, on respiratory activity before and after inhibition of neural activity in the RVM by dialysis of 10 mM muscimol, a GABAA-receptor agonist. Muscimol dialysis through probes that were placed along the ventral medullary surface from ∼1 mm rostral to the facial nucleus to ∼0.5 mm caudal to the facial nucleus augmented the respiratory inhibition associated with acute increases in blood pressure. No similar enhancement of respiratory inhibition after phenylephrine treatment was seen in six control animals that did not receive muscimol dialysis. We conclude that the piglet RVM participates in cardiorespiratory interactions and that dysfunction of homologous regions in the human infant could lead to cardiorespiratory instability and may be involved in the pathogenesis of sudden infant death syndrome.

APA, Harvard, Vancouver, ISO, and other styles

39

Sumińska-Ziemann, Barbara, Tomasz Gos, and Zbigniew Jankowski. "The role of respiratory failure caused by congenital central nervous system abnormalities and the effect of β-casomorphins in sudden infant death syndrome pathogenesis." Archives of Forensic Medicine and Criminology 2 (2015): 99–111. http://dx.doi.org/10.5114/amsik.2015.53226.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Curran, A. K., L. Xia, J. C. Leiter, and D. Bartlett. "Elevated body temperature enhances the laryngeal chemoreflex in decerebrate piglets." Journal of Applied Physiology 98, no. 3 (March 2005): 780–86. http://dx.doi.org/10.1152/japplphysiol.00906.2004.

Full text

Abstract:

Hyperthermia and reflex apnea may both contribute to sudden infant death syndrome (SIDS). Therefore, we investigated the effect of increased body temperature on the inhibition of breathing produced by water injected into the larynx, which elicits the laryngeal chemoreflex (LCR). We studied decerebrated, vagotomized, neonatal piglets aged 3–15 days. Blood pressure, end-tidal CO2, body temperature, and phrenic nerve activity were recorded. To elicit the LCR, we infused 0.1 ml of distilled water through a polyethylene tube passed through the nose and positioned just rostral to the larynx. Three to five LCR trials were performed with the piglet at normal body temperature. The animal's core body temperature was raised by ∼2.5°C, and three to five LCR trials were performed before the animal was cooled, and three to five LCR trials were repeated. The respiratory inhibition associated with the LCR was substantially prolonged when body temperature was elevated. Thus elevated body temperature may contribute to the pathogenesis of SIDS by increasing the inhibitory effects of the LCR.

APA, Harvard, Vancouver, ISO, and other styles

41

Highet, Amanda R., Anne M. Berry, Karl A. Bettelheim, and Paul N. Goldwater. "The frequency of molecular detection of virulence genes encoding cytolysin A, high-pathogenicity island and cytolethal distending toxin of Escherichia coli in cases of sudden infant death syndrome does not differ from that in other infant deaths and healthy infants." Journal of Medical Microbiology 58, no. 3 (March 1, 2009): 285–89. http://dx.doi.org/10.1099/jmm.0.005322-0.

Full text

Abstract:

Consistent pathological findings in sudden infant death syndrome (SIDS) are seen which display similarities to the pathogenesis of toxaemic shock and/or sepsis. A key candidate infectious agent that is possibly involved is Escherichia coli, given its universal early colonization of the intestinal tract of infants and an increased frequency of toxigenic and mouse-lethal isolates from SIDS compared with comparison infants. An explanation for these findings has yet to be identified. Using PCR, we screened E. coli isolates from 145 SIDS and 101 dead control and healthy infants for three new candidate pathogenicity-related genes: clyA (cytolysin A), irp2 [high-pathogenicity island (HPI)-specific gene] and cdt (cytolethal distending toxin). The results failed to show a positive correlation with SIDS, instead proving that clyA and irp2 genes were common to the infant intestinal E. coli. Interestingly we observed a high rate of carriage of these two potentially pathogenic genes in E. coli from healthy infants in the absence of diarrhoeal disease, and we report that in a number of cases, the detection of HPI-specific genes was predictable by serotype. Despite the lack of associations defined so far, there remains the likelihood that genetic determinants influence the interactions between E. coli and the host, so these factors may be part of the multi-factorial aspect of SIDS.

APA, Harvard, Vancouver, ISO, and other styles

42

Bychkova, I. Yu, Kh A. Abduvosidov, and V. V. Abduvosidov. "The role of hypoxia in the pathogenesis of congenital hyperplasia of blood vessels in the head and neck in children (literature review)." Acta Biomedica Scientifica 7, no. 1 (March 17, 2022): 37–47. http://dx.doi.org/10.29413/abs.2022-7.1.5.

Full text

Abstract:

To date, scientists have found that stress plays an important role in the formation of congenital malformations. It can be caused by the influence of negative environmental factors on the pregnant woman or by her own diseases. One of the consequences of stress is hypoxia. It can be acute and chronic, and can have a negative impact both during pregnancy and during childbirth. They also distinguish local and general hypoxia. The consequences of the negative impact of oxygen deficiency on the embryo and fetus can manifest itself both in utero and after birth, leading to various kinds of congenital malformations, diseases, and sometimes fetal death, or increase the risk of sudden infant death syndrome. Hyperplasia of blood vessels, the so-called children’s hemangiomas, develops both in utero, especially with chronic fetal hypoxia, and during childbirth. It develops due to insufficient blood supply and oxygen deficiency in various parts of the body, most often in the head and neck. In an embryo under conditions of hypoxia, tachycardia develops – with an increase in heart rate and, if it is ineffective, local vasodilation occurs. Only then, under the condition of continuing hypoxia, does an increase in the number of blood vessels develop. This often leads to the formation of hyperplasia of the blood vessels, the so-called children’s hemangiomas.This pathology is quite common, especially among fair-skinned children, which makes its study, in particular the factors that cause this pathology, relevant today.

APA, Harvard, Vancouver, ISO, and other styles

43

Goldstein, Richard D., Carter R. Petty, Sue E. Morris, Melanie Human, Hein Odendaal, Amy Elliott, Deb Tobacco, et al. "Pre-loss personal factors and prolonged grief disorder in bereaved mothers." Psychological Medicine 49, no. 14 (November 9, 2018): 2370–78. http://dx.doi.org/10.1017/s0033291718003264.

Full text

Abstract:

AbstractBackgroundIdentifying characteristics of individuals at greatest risk for prolonged grief disorder (PGD) can improve its detection and elucidate the etiology of the disorder. The Safe Passage Study, a study of women at high risk for sudden infant death syndrome (SIDS), prospectively examined the psychosocial functioning of women while monitoring their healthy pregnancies. Mothers whose infants died of SIDS were followed in bereavement.MethodsPre-loss data were collected from 12 000 pregnant mothers and analyzed for their associations with grief symptoms and PGD in 50 mothers whose infants died from SIDS, from 2 to 48 months after their infant's death, focusing on pre-loss risk factors of anxiety, depression, alcohol use, maternal age, the presence of other living children in the home, and previous child loss.ResultsThe presence of any four risk factors significantly predicted PGD for 24 months post-loss (p < 0.003); 2–3 risk factors predicted PGD for 12 months (p = 0.02). PGD rates increased in the second post-loss year, converging in all groups to approximately 40% by 3 years. Pre-loss depressive symptoms were significantly associated with PGD. Higher alcohol intake and older maternal age were consistently positively associated with PGD. Predicted risk scores showed good discrimination between PGD and no PGD 6–24 months after loss (C-statistic = 0.83).ConclusionsA combination of personal risk factors predicted PGD in 2 years of bereavement. There is a convergence of risk groups to high rates at 2–3 years, marked by increased PGD rates in mothers at low risk. The risk factors showed different effects on PGD.

APA, Harvard, Vancouver, ISO, and other styles

44

Mayer, C. A., J. M. Di Fiore, R. J. Martin, and P. M. MacFarlane. "Vulnerability of neonatal respiratory neural control to sustained hypoxia during a uniquely sensitive window of development." Journal of Applied Physiology 116, no. 5 (March 1, 2014): 514–21. http://dx.doi.org/10.1152/japplphysiol.00976.2013.

Full text

Abstract:

The first postnatal weeks represent a period of development in the rat during which the respiratory neural control system may be vulnerable to aberrant environmental stressors. In the present study, we investigated whether sustained hypoxia (SH; 11% O2) exposure starting at different postnatal ages differentially modifies the acute hypoxic (HVR) and hypercapnic ventilatory response (HCVR). Three different groups of rat pups were exposed to 5 days of SH, starting at either postnatal age 1 (SH1–5), 11 (SH11–15), or 21 (SH21–25) days. Whole body plethysmography was used to assess the HVR and HCVR the day after SH exposure ended. The primary results indicated that 1) the HVR and HCVR of SH11–15 rats were absent or attenuated (respectively) compared with age-matched rats raised in normoxia; 2) there was a profoundly high (∼84% of pups) incidence of unexplained mortality in the SH11–15 rats; and 3) these phenomena were unique to the SH11–15 group with no comparable effect of the SH exposure on the HVR, HCVR, or mortality in the younger (SH1–5) or older (SH21–25) rats. These results share several commonalities with the risk factors thought to underlie the etiology of sudden infant death syndrome, including 1) a vulnerable neonate; 2) a critical period of development; and 3) an environmental stressor.

APA, Harvard, Vancouver, ISO, and other styles

45

Darnall, Robert A., Robert W. Schneider, Christine M. Tobia, and Kathryn G. Commons. "Eliminating medullary 5-HT neurons delays arousal and decreases the respiratory response to repeated episodes of hypoxia in neonatal rat pups." Journal of Applied Physiology 120, no. 5 (March 1, 2016): 514–25. http://dx.doi.org/10.1152/japplphysiol.00560.2014.

Full text

Abstract:

Arousal from sleep is a critical defense mechanism when infants are exposed to hypoxia, and an arousal deficit has been postulated as contributing to the etiology of the sudden infant death syndrome (SIDS). The brainstems of SIDS infants are deficient in serotonin (5-HT) and tryptophan hydroxylase (TPH) and have decreased binding to 5-HT receptors. This study explores a possible connection between medullary 5-HT neuronal activity and arousal from sleep in response to hypoxia. Medullary raphe 5-HT neurons were eliminated from neonatal rat pups with intracisterna magna (CM) injections of 5,7-dihydroxytryptamine (DHT) at P2-P3. Each pup was then exposed to four episodes of hypoxia during sleep at three developmental ages (P5, P15, and P25) to produce an arousal response. Arousal, heart rate, and respiratory rate responses of DHT-injected pups were compared with pups that received CM artificial cerebrospinal fluid (aCSF) and those that received DHT but did not have a significant reduction in medullary 5-HT neurons. During each hypoxia exposure, the time to arousal from the onset of hypoxia (latency) was measured together with continuous measurements of heart and respiratory rates, oxyhemoglobin saturation, and chamber oxygen concentration. DHT-injected pups with significant losses of medullary 5-HT neurons exhibited significantly longer arousal latencies and decreased respiratory rate responses to hypoxia compared with controls. These results support the hypothesis that in newborn and young rat pups, 5-HT neurons located in the medullary raphe contribute to the arousal response to hypoxia. Thus alterations medullary 5-HT mechanisms might contribute to an arousal deficit and contribute to death in SIDS infants.

APA, Harvard, Vancouver, ISO, and other styles

46

Abu-Shaweesh, Jalal M. "Activation of central adenosine A2A receptors enhances superior laryngeal nerve stimulation-induced apnea in piglets via a GABAergic pathway." Journal of Applied Physiology 103, no. 4 (October 2007): 1205–11. http://dx.doi.org/10.1152/japplphysiol.01420.2006.

Full text

Abstract:

Activation of the laryngeal mucosa results in apnea that is mediated through, and can be elicited via electrical stimulation of, the superior laryngeal nerve (SLN). This potent inhibitory reflex has been suggested to play a role in the pathogenesis of apnea of prematurity and sudden infant death syndrome, and it is attenuated by theophylline and blockade of GABAA receptors. However, the interaction between GABA and adenosine in the production of SLN stimulation-induced apnea has not been previously examined. We hypothesized that activation of adenosine A2A receptors will enhance apnea induced by SLN stimulation while subsequent blockade of GABAA receptors will reverse the effect of A2A receptor activation. The phrenic nerve responses to increasing levels of SLN stimulation were measured before and after sequential intracisternal administration of the adenosine A2A receptor agonist CGS ( n = 10) and GABAA receptor blocker bicuculline ( n = 7) in ventilated, vagotomized, decerebrate, and paralyzed newborn piglets. Increasing levels of SLN stimulation caused progressive inhibition of phrenic activity and lead to apnea during higher levels of stimulation. CGS caused inhibition of baseline phrenic activity, hypotension, and enhancement of apnea induced by SLN stimulation. Subsequent bicuculline administration reversed the effects of CGS and prevented the production of apnea compared with control at higher SLN stimulation levels. We conclude that activation of adenosine A2A receptors enhances SLN stimulation-induced apnea probably via a GABAergic pathway. We speculate that SLN stimulation causes endogenous release of adenosine that activates A2A receptors on GABAergic neurons, resulting in the release of GABA at inspiratory neurons and subsequent respiratory inhibition.

APA, Harvard, Vancouver, ISO, and other styles

47

Staines, Donald R. "Postulated Vasoactive Neuropeptide Autoimmunity in Fatigue-Related Conditions: A Brief Review and Hypothesis." Clinical and Developmental Immunology 13, no. 1 (2006): 25–39. http://dx.doi.org/10.1080/17402520600568252.

Full text

Abstract:

Disorders such as chronic fatigue syndrome (CFS) and gulf war syndrome (GWS) are characterised by prolonged fatigue and a range of debilitating symptoms of pain, intellectual and emotional impairment, chemical sensitivities and immunological dysfunction. Sudden infant death syndrome (SIDS) surprisingly may have certain features in common with these conditions. Post-infection sequelae may be possible contributing factors although ongoing infection is unproven. Immunological aberration may prove to be associated with certain vasoactive neuropeptides (VN) in the context of molecular mimicry, inappropriate immunological memory and autoimmunity.Adenylate cyclase-activating VNs including pituitary adenylate cyclase-activating polypeptide (PACAP), vasoactive intestinal peptide (VIP) and calcitonin gene-related peptide (CGRP) act as hormones, neurotransmitters, neuroregulators, immune modulators and neurotrophic substances. They and their receptors are potentially immunogenic. VNs are widely distributed in the body particularly in the central and peripheral nervous systems and have been identified in the gut, adrenal gland, blood cells, reproductive system, lung, heart and other tissues. They have a vital role in maintaining cardio-respiratory function, thermoregulation, memory, concentration and executive functions such as emotional responses including social cues and appropriate behaviour. They are co-transmitters for a number of neurotransmitters including acetylcholine and gaseous transmitters, are potent immune regulators with primarily anti-inflammatory activity, and have a significant role in protection of the nervous system against toxic assault as well as being important in the maintenance of homeostasis.This paper describes a biologically plausible mechanism for the development of certain fatigue-related syndromes based on loss of immunological tolerance to these VNs or their receptors following infection, other events or de novo resulting in significant pathophysiology possibly mediated via CpG fragments and heat shock (stress) proteins. These conditions extend the public health context of autoimmunity and VN dysregulation and have implications for military medicine where radiological, biological and chemical agents may have a role in pathogenesis. Possible treatment and prevention options are considered.

APA, Harvard, Vancouver, ISO, and other styles

48

Barrett, Karlene T., Shabih U. Hasan, Morris H. Scantlebury, and Richard J. A. Wilson. "Impaired neonatal cardiorespiratory responses to hypoxia in mice lacking PAC1 or VPAC2 receptors." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 316, no. 5 (May 1, 2019): R594—R606. http://dx.doi.org/10.1152/ajpregu.00250.2018.

Full text

Abstract:

The stress peptide pituitary adenylate cyclase activating polypeptide (PACAP) and its specific receptor PACAP type 1 receptor (PAC1) have been implicated in sudden infant death syndrome (SIDS). PACAP is also critical to the neonatal cardiorespiratory response to homeostatic stressors identified in SIDS, including hypoxia. However, which of PACAP’s three receptors, PAC1, vasoactive intestinal peptide receptor type 1 (VPAC1), and/or vasoactive intestinal peptide receptor type 2 (VPAC2), are involved is unknown. In this study, we hypothesized that PAC1, but not VPAC2, is involved in mediating the cardiorespiratory response to hypoxia during neonatal development. To test this hypothesis, head-out plethysmography and surface ECG electrodes were used to assess the cardiorespiratory variables of unanesthetized postnatal day 4 PAC1 and VPAC2-knockout (KO) and wild-type (WT) mice in response to a 10% hypoxic challenge. Our results demonstrate that compared with WT pups, the early and late hypoxic rate of expired CO2 (V̇co2), V̇co2 and ventilatory responses were blunted in PAC1-KO neonates, and during the posthypoxic period, minute ventilation (V̇e), V̇co2 and heart rate were increased, while the increase in apneas normally associated with the posthypoxic period was reduced. Consistent with impaired cardiorespiratory control in these animals, the V̇e/V̇co2 slope was reduced in PAC1-KO pups, suggesting that breathing was inappropriately matched to metabolism. In contrast, VPAC2-KO pups exhibited elevated heart rate variability during hypoxia compared with WT littermates, but the effects of the VPAC2-KO genotype on breathing were minimal. These findings suggest that PAC1 plays the principal role in mediating the cardiorespiratory effects of PACAP in response to hypoxic stress during neonatal development and that defective PACAP signaling via PAC1 may contribute to the pathogenesis of SIDS.

APA, Harvard, Vancouver, ISO, and other styles

49

Takeuchi, Suguru, Jun-ichi Kawada, Kazuhiro Horiba, Makoto yamaguchi, Toshihiko Okumura, Takako Suzuki, Yuka Torii, et al. "1224. Investigation of Infectious Etiologies in the Lower Respiratory Tract from Pediatric Patients with Unexpected Cardiopulmonary Deterioration using Next-Generation Sequencing." Open Forum Infectious Diseases 7, Supplement_1 (October 1, 2020): S633. http://dx.doi.org/10.1093/ofid/ofaa439.1409.

Full text

Abstract:

Abstract Background In pediatric patients, unexpected cardiopulmonary deterioration with or without following cardiopulmonary arrest (CPA) are rare events, but can be caused by any of several etiologies, including infectious diseases. The most common cause of out-of-hospital CPA in children ≤12 years old was sudden infant death syndrome (SIDS), whereas infectious diseases were responsible for approximately 10% of the CPA cases. However, the role of infection may have been underestimated as triggers of SIDS or CPA. This study aimed to investigate the infectious etiologies in pediatric patients with unexpected cardiopulmonary deterioration using next-generation sequencing (NGS). Methods A total of 16 pediatric patients who were admitted to the pediatric intensive care unit with unexpected cardiopulmonary deterioration with or without following CPA were enrolled. Ten bronchoalveolar fluid (BALF) and six transtracheal aspirates (TTA) samples obtained in the acute phase were used to prepare NGS libraries. The libraries were sequenced on HiSeq and analyzed using metagenome analysis tools. Results In ten of 16 patients, one or more bacterial/viral pathogens were detected in the BALF or TTA specimens using NGS. Compared to the conventional culture and viral antigen test results, an additional 6 bacterial (e.g., Chlamydia trachomatis) and 4 viral pathogens (e.g., coxsackievirus A6 and human coronavirus NL63) were identified by NGS in four of ten patients in whom no causative pathogen had been identified by conventional culture and viral antigen tests. A summary of the detected pathogens is listed in Table 1. Notably, sequencing results allowed us to define genotypes for all of the detected viruses in a single NGS assay per patient. Furthermore, based on phylogenetic analysis of the VP1 region, the coxsackievirus A6 strain detected in this study belongs to lineage E2 and harbors an amino acid change (T283A), a substitution that has potential to cause severe illness. Table 1 Conclusion Our results suggest that viral and bacterial infection are common triggers in unexpected cardiopulmonary deterioration in pediatric patients. NGS has the potential to contribute to the clarification of the etiology of pediatric critical illness. Disclosures All Authors: No reported disclosures

APA, Harvard, Vancouver, ISO, and other styles

50

Qu, Dong, Peter Schürmann, Thomas Rothämel, Thilo Dörk, and Michael Klintschar. "Variants in genes encoding the SUR1-TRPM4 non-selective cation channel and sudden infant death syndrome (SIDS): potentially increased risk for cerebral edema." International Journal of Legal Medicine, April 26, 2022. http://dx.doi.org/10.1007/s00414-022-02819-9.

Full text

Abstract:

AbstractIncreasing evidence suggests that brain edema might play an important role in the pathogenesis of sudden infant death syndrome (SIDS) and that variants of genes for cerebral water channels might be associated with SIDS. The role of the sulfonylurea receptor 1 (SUR1)–transient receptor potential melastatin 4 (TRPM4) non-selective cation channel in cerebral edema was demonstrated by extensive studies. Therefore, we hypothesized that variants at genes of the SUR1-TRPM4 channel complex might be linked to SIDS. Twenty-four polymorphisms in candidate genes involved in the SUR1-TRPM4 non-selective cation channel were investigated in 185 SIDS cases and 339 controls. One (rs11667393 in TRPM4) of these analyzed SNPs reached nominal significance regarding an association with SIDS in the overall analysis (additive model: p = 0.015, OR = 1.438, 95% CI = 1.074–1.925; dominant model: p = 0.036; OR = 1.468, 95% CI = 1.024–2.106). In the stratified analysis, further 8 variants in ABCC8 (encoding SUR1) or TRPM4 showed pronounced associations. However, none of the results remained significant after correction for multiple testing. This preliminary study has provided the first evidence for a genetic role of the SUR1-TRPM4 complex in the etiology of SIDS, and we suggest that our initial results should be evaluated by further studies.

APA, Harvard, Vancouver, ISO, and other styles

Journal articles on the topic 'Sudden infant death syndrome – Etiology; Sudden infant death syndrome – Pathogenesis'

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles