Sudden Death (Book 2 In The Population Control)

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  1. The Population Bomb - Wikipedia
  2. Overpopulation (Book 1 In The Population Control)
  3. The Book That Incited a Worldwide Fear of Overpopulation
  4. The Sudden Infant Death Syndrome

American Academy of Pediatrics. Vege A, Ole Rognum T. Sudden infant death syndrome, infection and inflammatory responses. Infection and sudden unexpected death in infancy: A perspective on neuropathologic findings in victims of the sudden infant death syndrome: The triple risk hypotheses in sudden infant death syndrome.

Hazardous infant and early childhood sleeping environments and death scene examination. J Clin Forensic Med. Infant death scene investigation and the assessment of potential risk factors for asphyxia: Impact of changes in infant death classification on the diagnosis of sudden infant death syndrome. Clin Pediatr Phila ; Multiple serotonergic brainstem abnormalities in sudden infant death syndrome. Unsafe sleep practices and an analysis of bedsharing among infants dying suddenly and unexpectedly: Factors potentiating the risk of sudden infant death syndrome associated with the prone position.

The Population Bomb - Wikipedia

Secular changes in sleep position during infancy: Prone sleeping position increases the risk of SIDS in the day more than at night. Mother-infant cosleeping, breastfeeding and sudden infant death syndrome: Am J Phys Anthropol. Effects of prematurity on heart rate control: Expert Rev Cardiovasc Ther.

Population-based recurrence risk of sudden infant death syndrome compared with other infant and fetal deaths. Sudden infant death syndrome: Am J Med Genet A. Sudden infant death syndrome and sleeping position in pre-term and low birth weight infants: Prematurity, sudden infant death syndrome, and age of death. Major epidemiological changes in sudden infant death syndrome: Smoking and the sudden infant death syndrome: The effect of maternal smoking and drinking during pregnancy upon 3 H-nicotine receptor brainstem binding in infants dying of the sudden infant death syndrome: Postnatal depression and SIDS: Barriers to following the supine sleep recommendation among mothers at four centers for the Women, Infants, and Children Program.

Leiter JC, Bohm I.

Mechanisms of pathogenesis in the sudden infant death syndrome. Autonomic control during sleep and risk for sudden death in infancy. Sudden infant death syndrome, virus infections and cytokines.

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Development of thermoregulation in infancy: Identifying infants at risk for sudden infant death syndrome. Medullary serotonergic network deficiency in the sudden infant death syndrome: J Neuropathol Exp Neurol. Tragic and sudden death: Subtle autonomic and respiratory dysfunction in sudden infant death syndrome associated with serotonergic brainstem abnormalities: Dynamics of respiratory patterning in normal infants and infants who subsequently died of the sudden infant death syndrome.

Sinus tachycardia in term infants preceding sudden infant death. Sudden death in infants sleeping on polystyrene-filled cushions. Skadberg BT, Markestad T. Consequences of getting the head covered during sleep in infancy. Thach BT, Lijowska A. Apparent life-threatening events and sudden infant death on a monitor. Characterization of successful and failed autoresuscitation in human infants, including those dying of SIDS. Pulmonary neuroendocrine cells and neuroepithelial bodies in sudden infant death syndrome: Vitreous humor hypoxanthine levels in SIDS and infectious death. Vascular endothelial growth factor in the cerebrospinal fluid of infants who died of sudden infant death syndrome: Brain-stem and adrenal abnormalities in the sudden-infant-death syndrome.

Am J Clin Pathol. Machaalani R, Waters KA. Neuronal cell death in the sudden infant death syndrome brainstem and associations with risk factors.

Inspired CO 2 and O 2 in sleeping infants re-breathing from bedding: Neurophysiological mechanisms of sleep and wakefulness: Sequential arousal and airway-defensive behavior of infants in asphyxial sleep environments. Incomplete arousal processes in infants who were victims of sudden death. Sleep state organization in normal infants and victims of the sudden infant death syndrome. Sleep and cardiorespiratory characteristics of infant victim of sudden death: Respiratory rhythm generation during gasping depends on persistent sodium current. Gasping activity in vitro: Maintenance of gasping and restoration of eupnea after hypoxia is impaired following blockers of alpha1-adrenergic receptors and serotonin 5-HT2 receptors.

A clinical comparison of SIDS and explained sudden infant deaths: Gasping and other cardiorespiratory patterns during sudden infant deaths. An animal model of life-threatening hyperthermia during infancy. Cardiorespiratory events recorded on home monitors: Cardiorespiratory behavior during sleep in fullterm and preterm neonates at comparable postconceptional term ages. Interactions between sleeping position and feeding on cardiorespiratory activity in preterm infants. Interaction between bedding and sleeping position in the sudden infant death syndrome: Combination, complementarity and automatic control: Sandy rated it it was ok Jan 18, Jeniffer Murray-fields rated it it was ok Apr 03, Clarke added it Mar 24, Jessica marked it as to-read Apr 01, Policar marked it as to-read Jul 15, Natasha marked it as to-read Aug 21, Olivia Thomas marked it as to-read Jun 20, Lorena marked it as to-read Aug 20, Jessica Smith marked it as to-read Oct 18, Sonia Rudolph marked it as to-read Aug 02, Joy Jensen marked it as to-read Jun 04, Dee added it Feb 12, Out of cases, cases did not have an accurate age record.

In the remaining cases, the ages ranged from 15 to 52 years old Figure 1.

Overpopulation (Book 1 In The Population Control)

The case number was relatively small for ages 15—24 years only 1 victim at age 15 years but started to rise drastically from the age of 25 years 36 victims at age 25 and then peaked at the age of 30 years 59 victims at age The case number was relatively stable at ages 31—40 years and dropped sharply after 41 years 21 victims at age 41 and dropped further with increase in age. Victims aged 21 to 40 years accounted for SUNDS occurred throughout the year with a mean occurrence of 65 cases per month.

The monthly distribution of Emergency fever patients cases in three hospitals in the studied area during — The majority of SUNDS victims were poorly educated workers who engaged in manual labor blue-collar workers except for 4 cases with history of higher education and administrative position. In cases, the largest numbers were construction workers 21 cases and electronic appliance factory workers 19 cases. The percentage of blue-collar workers in the general population is not available. Sixty five SUNDS cases had reports from witnesses such as spouses who could identify presence or absence of symptoms at the time of death or immediately prior to death.

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According to these descriptions, all 65 died instantly or within a few minutes of the onset of distress in sleep. Forty-nine out of 65 cases of sudden death occurred with obvious manifestations before death Table 2. All cases died in their sleep.

The Book That Incited a Worldwide Fear of Overpopulation

The time of death in witnessed cases was accurately provided. The number of victims and the span of corresponding time of death were as follows: There were 2 cases that died in their sleep at about We traced four generations in two families with history of SUNDS and each case revealed male victims in the second and third generations at ages between 17 and 38 years. In one family, surviving relatives did not show clear evidence of significant cardiac structural defects but two male brothers at the age of 28 and 30 years, respectively had ECGs with unusually deep inferior Q waves in leads II, III, and aVF.

One was a mis-sense mutation CT RW, in exon 26, detected in the 46 th case which was previously reported in Brugada syndrome. The other is a novel synonymous mutation GA AA, in exon 18, detected in the 63 rd case. The genotype and allele frequencies of the identified SNPs are summarizd in Table 3.

In northeast Thailand the annual mortality of death was reported to be 38 per , people aged 20—49 4 , which is the highest reported incidence in the world. However, the figure may have been overestimated because the cause of death in these cases was not confirmed by autopsies and microscopic examination. China is geographically close to Thailand and might also be expected to have a high occurrence rate. This study showed that the mean annual mortality of SUNDS in the three regions in the past three years was about 0. Based on these findings, we infer that the occurrence rate of the sudden death in southern China is about 1.

The Sudden Infant Death Syndrome

Although the rate is not as high as other reported rates, the absolute number of annual SUNDS cases in China may be considerable because of the large population. Young males between the ages of 21 and 40, and especially those around 30, are dominant in the SUNDS population. The population aged 21—40 may be confronted with the largest stress in both psychological and physical aspects, and perhaps subjects are at particular risk due to high levels of fatigue. From this point of view, the cause of some SUNDS cases may be focused on the factors related to overwork.

Alternatively, the age of incidence may result from developmental factors combined with a genetic predisposition. Male victims occupied Valladares found that during the rapid eye movement sleep, the male cardiac vagal tone significantly declined while sympathetic nerve activity markedly increased as compared with women and that the gender differences may be closely related to higher incidence of heart related problems in males 8.

SUNDS has been known to occur frequently in Southeast Asian regions with tropical or subtropical climates and hot weather.