Publications by authors named "Paul Goldwater"

Article Synopsis
  • Recent research into Sudden Infant Death Syndrome (SIDS) suggests that metabolic acidosis and sepsis are significant factors, challenging the traditional brain-centered theories that have dominated the field for decades.
  • Analysis of various studies indicates that infections might play a crucial role, as many SIDS risk factors are tied to infection, which could lead to organ failure and respiratory issues in infants.
  • The paper advocates for including specific metabolic tests (like pH and bicarbonate levels) in autopsies of unexpected child deaths to better understand the underlying causes of SIDS.
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From the earliest publications on cot death or sudden infant death syndrome (SIDS) through to this day, clinical pathology and epidemiology have strongly featured infection as a constant association. Despite mounting evidence of the role of viruses and common toxigenic bacteria in the pathogenesis of SIDS, a growing school of thought featuring a paradigm based on the triple risk hypothesis that encompasses vulnerability through deranged homoeostatic control of arousal and/or cardiorespiratory function has become the mainstream view and now dominates SIDS research. The mainstream hypothesis rarely acknowledges the role of infection despite its notional potential role as a cofactor in the triple hit idea.

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Unlabelled: This paper presents a timely and constructive critique of mainstream SIDS research. It is concerning that twenty-first century medical science has not provided an answer to the tragic enigma of SIDS. The paper helps explain why this is so and illustrates possible shortcomings in the investigation of Sudden Infant Death Syndrome/Sudden Unexplained Infant Death (SIDS/SUID) by mainstream researchers.

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Lymphocytic choriomeningitis virus (LCMV) is a ubiquitous virus carried by rodents. It causes human disease through contact with infectious mouse faeces, urine or secretions. The virus initially infects the human respiratory tract and lungs and produces typical viral symptoms and signs.

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The etiology of sudden infant death syndrome (SIDS) still remains unclear. This situation would seem unprecedented for 21st-century medical science. This article explores scientific fields that have not been largely considered in investigating the etiology of SIDS so far.

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Objective: The goal of the present investigation is to analyze thymus, brain, heart, liver, and kidney weights in SIDS victims compared to controls.

Background: Epidemiologic risk factors for SIDS (eg, male gender, genetic, obstetric, environmental, smoke exposure, nonbreastfeeding, etc.) are consistent with an infectious process underlying many of these deaths.

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Mainstream researchers explain the etiology of SIDS with the cardiorespiratory paradigm. This has been the focus of intense study for many decades without providing consistent supporting data to link CNS findings to epidemiological risk factors or to the usual clinicopathological findings. Despite this, and the apparent oversight of the link between prone sleep position and respiratory infection, papers citing CNS, cardiac and sleep arousal findings continue to be published.

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Recent findings suggest that infection (and sepsis) stand alone as the only plausible mechanism of causation of sudden infant death syndrome (SIDS) and accordingly achieves congruence with all clinicopathological and epidemiological findings. This review examines the role of infection in the pathogenesis of SIDS in the context of the major risk factor of prone sleep position. The study explores how sleep position could interact with the immune system and inflammatory response vagal neural connections, which could play key roles in gut and immune homeostasis.

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Objective: To assess whether features of the infant intestinal microbiome, including the carriage of toxigenic bacteria, are associated with sudden infant death syndrome (SIDS).

Study Design: We undertook a case-controlled analysis of fecal microbiology in SIDS. Fecal material was obtained from 44 cases and 44 aged-matched controls.

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Despite decades of investigation and millions of dollars spent, the cause of sudden infant death syndrome (SIDS) eludes researchers. It is timely therefore to reconsider the reasons for this failure and to explore how research might go forward with better prospects. This review assesses SIDS research in the context of clinicopathological and epidemiological features and determines that only infection attains congruence.

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This review examines the association of strains of Escherichia coli with sudden infant death syndrome (SIDS) and the possible role these bacteria play in this enigmatic condition. The review addresses evidence for E. coli in SIDS infants, potential sources of E.

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The gut microbiome influences the development of the immune system of young mammals; the establishment of a normal gut microbiome is thought to be important for the health of the infant during its early development. As the role of bacteria in the causation of sudden infant death syndrome (SIDS) is backed by strong evidence, the balance between host immunity and potential bacterial pathogens is likely to be pivotal. Bacterial colonization of the infant colon is influenced by age, mode of delivery, diet, environment, and antibiotic exposure.

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The role of bacteria in the causation of sudden infant death syndrome (SIDS) is gaining acceptance. Mainstream research favouring respiratory compromise has failed to provide a plausible pathogenetic mechanism despite many years of investigation and thousands of research papers. Bacterial colonisation of the colon of the human infant is influenced by many factors including age, mode of delivery, diet, environment, and antibiotic exposure.

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Aim: This study aims to examine single nucleotide polymorphism (SNP) associations with cerebral palsy in a multi-variable analysis adjusting for potential clinical confounders and to assess SNP-SNP and SNP-maternal infection interactions as contributors to cerebral palsy.

Methods: A case control study including 587 children with cerebral palsy and 1154 control children without cerebral palsy. Thirty-nine candidate SNPs were genotyped in both mother and child.

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Pediatric infectious disease clinicians in industrialized countries may encounter iatrogenically transmitted HIV, hepatitis B virus, and hepatitis C virus infections in refugee children from Central Asia, Southeast Asia, and sub-Saharan Africa. The consequences of political collapse and/or civil war-work migration, prostitution, intravenous drug use, defective public health resources, and poor access to good medical care-all contribute to the spread of blood-borne viruses. Inadequate infection control practices by medical establishments can lead to iatrogenic infection of children.

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Unlabelled: A number of maternal and perinatal factors to increase an infant's risk of sudden infant death syndrome (SIDS) have been found in past investigations. We analysed data for potential SIDS risk factors including the presence of complications or conditions considered as detrimental to the infant's or mother's health. The data for 118 SIDS cases and 227 matched controls were obtained from a state pregnancy outcome unit.

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Objective: Intrauterine infection is a risk factor for cerebral palsy. Previous work reported a high frequency of viral DNA in newborn screening cards from cerebral palsy cases and controls possibly due to contamination.

Methods: Retrospective case-control study using improved methodologies to minimize contamination during PCR-based detection of viral DNA sequences.

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Verotoxigenic Escherichia coli (VTEC) are a specialized group of E. coli that can cause severe colonic disease and renal failure. Their pathogenicity derives from virulence factors that enable the bacteria to colonize the colon and deliver extremely powerful toxins known as verotoxins (VT) or Shiga toxins (Stx) to the systemic circulation.

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Article Synopsis
  • This study examined genetic and epidemiologic risk factors for cerebral palsy (CP) in both mothers and children, focusing on a specific set of genetic variants known as single nucleotide polymorphisms (SNPs).
  • DNA from 587 CP cases and 1154 control pairs was analyzed to see if certain SNPs linked to thrombophilia, inflammation, and other risk factors could be associated with CP.
  • The results showed that while there were some marginal associations, mainly with the prothrombin gene mutation, no definitive links were found between the other candidate SNPs and CP, suggesting that previous associations might have been due to statistical errors in earlier studies.
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Objective: To estimate epidemiologic risk factors for cerebral palsy.

Methods: Data were collected by linkage to state-based perinatal repositories and cerebral palsy registers and using a maternal questionnaire. The cohort included 587 individuals with cerebral palsy and 1,154 non-cerebral palsy controls.

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Several theories of the underlying mechanisms of Sudden Infant Death Syndrome (SIDS) have been proposed. These theories have born relatively narrow beach-head research programs attracting generous research funding sustained for many years at expense to the public purse. This perspective endeavors to critically examine the evidence and bases of these theories and determine their plausibility; and questions whether or not a safe and reasoned hypothesis lies at their foundation.

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Reliable detection of viral DNA in stored newborn screening cards (NSC) would give important insight into possible silent infection during pregnancy and around birth. We sought a DNA extraction method with sufficient sensitivity to detect low copy numbers of viral DNA from small punch samples of NSC. Blank NSC were spotted with seronegative EDTA-blood and seropositive EBV EDTA-blood.

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