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Academic literature on the topic 'Asphyxia in the air'

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Published: 10 March 2023

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Journal articles on the topic "Asphyxia in the air"

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Xie, Ailiang, James B. Skatrud, David C. Crabtree, Dominic S. Puleo, Brian M. Goodman, and Barbara J. Morgan. "Neurocirculatory consequences of intermittent asphyxia in humans." Journal of Applied Physiology 89, no. 4 (October 1, 2000): 1333–39. http://dx.doi.org/10.1152/jappl.2000.89.4.1333.

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We examined the neurocirculatory and ventilatory responses to intermittent asphyxia (arterial O2 saturation = 79–85%, end-tidal Pco 2 =3–5 Torr above eupnea) in seven healthy humans during wakefulness. The intermittent asphyxia intervention consisted of 20-s asphyxic exposures alternating with 40-s periods of room-air breathing for a total of 20 min. Minute ventilation increased during the intermittent asphyxia period (14.2 ± 2.0 l/min in the final 5 min of asphyxia vs. 7.5 ± 0.4 l/min in baseline) but returned to the baseline level within 2 min after completion of the series of asphyxic exposures. Muscle sympathetic nerve activity increased progressively, reaching 175 ± 12% of baseline in the final 5 min of the intervention. Unlike ventilation, sympathetic activity remained elevated for at least 20 min after removal of the chemical stimuli (150 ± 10% of baseline in the last 5 min of the recovery period). Intermittent asphyxia caused a small, but statistically significant, increase in heart rate (64 ± 4 beats/min in the final 5 min of asphyxia vs. 61 ± 4 beats/min in baseline); however, this increase was not sustained after the return to room-air breathing. These data demonstrate that relatively short-term exposure to intermittent asphyxia causes sympathetic activation that persists after removal of the chemical stimuli. This carryover effect provides a potential mechanism whereby intermittent asphyxia during sleep could lead to chronic sympathetic activation in patients with sleep apnea syndrome.
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Morgan, B. J., D. C. Crabtree, M. Palta, and J. B. Skatrud. "Combined hypoxia and hypercapnia evokes long-lasting sympathetic activation in humans." Journal of Applied Physiology 79, no. 1 (July 1, 1995): 205–13. http://dx.doi.org/10.1152/jappl.1995.79.1.205.

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We studied ventilatory and neurocirculatory responses to combined hypoxia (arterial O2 saturation 80%) and hypercapnia (end-tidal CO2 + 5 Torr) in awake humans. This asphyxic stimulus produced a substantial increase in minute ventilation (6.9 +/- 0.4 to 20.0 +/- 1.5 l/min) that promptly subsided on return to room air breathing. During asphyxia, muscle sympathetic nerve activity (intraneural microelectrodes) increased to 220 +/- 28% of the room air baseline. Approximately two-thirds of this sympathetic activation persisted after return to room air breathing for the duration of our measurements (20 min in 8 subjects, 1 h in 2 subjects). In contrast, neither ventilation nor sympathetic outflow changed during time control experiments. A 20-min exposure to hyperoxic hypercapnia also caused a sustained increase in sympathetic activity, but, unlike the aftereffect of asphyxia, this effect was short lived and coincident with continued hyperpnea. In summary, relatively brief periods of asphyxic stimulation cause substantial increases in sympathetic vasomotor outflow that outlast the chemical stimuli. These findings provide a potential explanation for the chronically elevated sympathetic nervous system activity that accompanies sleep apnea syndrome.
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Brambrink, Ansgar M., Lee J. Martin, Daniel F. Hanley, Kyra J. Becker, Raymond C. Koehler, and Richard J. Traystman. "Effects of the AMPA Receptor Antagonist NBQX on Outcome of Newborn Pigs after Asphyxic Cardiac Arrest." Journal of Cerebral Blood Flow & Metabolism 19, no. 8 (August 1999): 927–38. http://dx.doi.org/10.1097/00004647-199908000-00012.

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In neonates, asphyxia is a common cause of neuronal injury and often results in seizures. The authors evaluated whether blockade of a-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors during asphyxia and early recovery with 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo-(F)-quinoxaline (NBQX) ameliorates neurologic deficit and histopathology in 1-week-old piglets. Anesthetized piglets were exposed to a sequence of 30 minutes of hypoxia, 5 minutes of room air ventilation, 7 minutes of airway occlusion, and cardiopulmonary resuscitation. Vehicle or NBQX was administered intravenously before asphyxia (30 mg/kg) and during the first 4 hours of recovery (15 mg/kg/h). Neuropathologic findings were evaluated at 96 hours of recovery by light microscopic and cytochrome oxidase histochemical study. Cardiac arrest occurred at 5 to 6 minutes of airway occlusion, and cardiopulmonary resuscitation restored spontaneous circulation independent of treatment modalities in about 2 to 3 minutes. Neurologic deficit over the 96-hour recovery period was not ameliorated by NBQX. Seizure activity began after 24 to 48 hours in 7 of 10 animals with vehicle and in 9 of 10 of animals with NBQX. In each group, four animals died in status epilepticus. Neuropathologic outcomes were not improved by NBQX. The density of remaining viable neurons was decreased in parietal cortex and putamen by NBQX treatment. Metabolic defects in cytochrome oxidase activity were worsened by NBQX treatment. Seizure activity during recovery was associated with reduced neuronal viability in neocortex and striatum in piglets from both groups that survived for 96 hours. This neonatal model of asphyxic cardiac arrest and resuscitation generates neurologic deficits, clinical seizure activity, and selective damage in regions of basal ganglia and sensorimotor cortex. In contrast to other studies in mature brain, AMPA receptor blockade with NBQX failed to protect against neurologic damage in the immature piglet and worsened postasphyxic histopathologic outcome in neocortex and putamen.
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Rzemieniec, J., E. Bratek, A. Wnuk, K. Przepiórska, E. Salińska, and M. Kajta. "Neuroprotective effect of 3,3’-Diindolylmethane against perinatal asphyxia involves inhibition of the AhR and NMDA signaling and hypermethylation of specific genes." Apoptosis 25, no. 9-10 (August 20, 2020): 747–62. http://dx.doi.org/10.1007/s10495-020-01631-3.

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Abstract Each year, 1 million children die due to perinatal asphyxia; however, there are no effective drugs to protect the neonatal brain against hypoxic/ischemic damage. In this study, we demonstrated for the first time the neuroprotective capacity of 3,3’-diindolylmethane (DIM) in an in vivo model of rat perinatal asphyxia, which has translational value and corresponds to hypoxic/ischemic episodes in human newborns. Posttreatment with DIM restored the weight of the ipsilateral hemisphere and normalized cell number in the brain structures of rats exposed to perinatal asphyxia. DIM also downregulated the mRNA expression of HIF1A-regulated Bnip3 and Hif1a which is a hypoxic marker, and the expression of miR-181b which is an indicator of perinatal asphyxia. In addition, DIM inhibited apoptosis and oxidative stress accompanying perinatal asphyxia through: downregulation of FAS, CASP-3, CAPN1, GPx3 and SOD-1, attenuation of caspase-9 activity, and upregulation of anti-apoptotic Bcl2 mRNA. The protective effects of DIM were accompanied by the inhibition of the AhR and NMDA signaling pathways, as indicated by the reduced expression levels of AhR, ARNT, CYP1A1, GluN1 and GluN2B, which was correlated with enhanced global DNA methylation and the methylation of the Ahr and Grin2b genes. Because our study provided evidence that in rat brain undergoing perinatal asphyxia, DIM predominantly targets AhR and NMDA, we postulate that compounds that possess the ability to inhibit their signaling are promising therapeutic tools to prevent stroke.
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Busija, D. W., and M. Wei. "Altered cerebrovascular responsiveness to N-methyl-D-aspartate after asphyxia in piglets." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 1 (July 1, 1993): H389—H394. http://dx.doi.org/10.1152/ajpheart.1993.265.1.h389.

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We examined effects of prior asphyxia and reventilation on pial arteriolar responses to arterial hypercapnia, topical application of forskolin, and topical application of N-methyl-D-aspartate (NMDA) in newborn pigs. Piglets were anesthetized and ventilated with a respirator. Pial arteriolar diameter was determined using a closed cranial window and intravital microscopy. After baseline diameter was determined, the respirator was turned off for 10 min. Then the respirator was turned on, and the piglet was ventilated for 4 h. At 1, 2, and 4 h after asphyxia, arteriolar diameter was determined during control conditions and during arterial hypercapnia (inspiration of 10% CO2 in air; n = 4), topical application of 2.4 x 10(-8) M forskolin (n = 6), and topical application of 10(-5) M NMDA (n = 6). At 1 h after asphyxia, arterial hypercapnia dilated pial arterioles by 39 +/- 3%, topical forskolin dilated pial arterioles by 24 +/- 3%, and NMDA dilated pial arterioles by 10 +/- 1%. For arterial hypercapnia and forskolin application, arteriolar responses were not different from 1 h at 2 and 4 h postasphyxia. In contrast, for NMDA, arteriolar responses were greater at 2 h (23 +/- 6%) and 4 h (30 +/- 5%) than at 1 h. In time-control animals, NMDA dilated arterioles by 20 +/- 5% at 1 h, by 24 +/- 8% at 2 h, and by 21 +/- 4% at 4 h (n = 5). Indomethacin administration (5 mg/kg iv) before asphyxia resulted in a 23 +/- 3% arteriolar dilation in response to NMDA at 1 h (n = 7).(ABSTRACT TRUNCATED AT 250 WORDS)
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Chaudhry, Samena, Magnus Harrison, and Martin S. Roth. "First aid: Airway, choking and asphyxia." BMJ 330, Suppl S3 (March 1, 2005): 0503100. http://dx.doi.org/10.1136/sbmj.0503100.

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Van Heeswijk, J. C. F., J. Van Pelt, and G. E. E. J. M. Van den Thillart. "Free fatty acid metabolism in the air-breathing African catfish (Clarias gariepinus) during asphyxia." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 141, no. 1 (May 2005): 15–21. http://dx.doi.org/10.1016/j.cbpb.2005.03.006.

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Fanos, V., A. Noto, T. Xanthos, M. Lussu, F. Murgia, L. Barberini, G. Finco, et al. "Metabolomics Network Characterization of Resuscitation after Normocapnic Hypoxia in a Newborn Piglet Model Supports the Hypothesis That Room Air Is Better." BioMed Research International 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/731620.

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Perinatal asphyxia is attributed to hypoxia and/or ischemia around the time of birth and may lead to multiorgan dysfunction. Aim of this research article is to investigate whether different metabolomic profiles occurred according to oxygen concentration administered at resuscitation. In order to perform the experiment, forty newborn piglets were subjected to normocapnic hypoxia and reoxygenation and were randomly allocated in 4 groups resuscitated with different oxygen concentrations, 18%, 21%, 40%, and 100%, respectively. Urine metabolic profiles at baseline and at hypoxia were analysed by1H-NMR spectroscopy and metabolites were also identified by multivariate statistical analysis. Metabolic pathways associations were also built up by ingenuity pathway analysis (IPA). Bioinformatics analysis of metabolites characterized the effect of metabolism in the 4 groups; it showed that the 21% of oxygen is the most “physiological” and appropriate concentration to be used for resuscitation. Our data indicate that resuscitation with 21% of oxygen seems to be optimal in terms of survival, rapidity of resuscitation, and metabolic profile in the present animal model. These findings need to be confirmed with metabolomics in human and, if so, the knowledge of the perinatal asphyxia condition may significantly improve.
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Lestari, Siti, Dyah Dwi Astuti, and Fachriza Malika Ramadhani. "Analisis Faktor Fetus dan Tali Pusat terhadap Risiko Asphyxia Perinatal di Surakarta." Jurnal Ilmu Keperawatan Anak 3, no. 1 (May 31, 2020): 16. http://dx.doi.org/10.32584/jika.v3i1.521.

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Asfiksia perinatal merujuk pada kekurangan oksigen selama persalinan, sehingga berpotensi menyebabkan kematian dan kecacatan. WHO memperkirakan 4 juta anak terlahir dengan asfiksia setiap tahun, dimana 1 juta di antaranya meninggal dan 1 juta anak bertahan hidup dengan gejala sisa neurologis yang parah. Penelitian ini bertujuan untuk menganalisis faktor risiko fetal dan tali pusat pada asfiksia neonatal.Penelitian dilakukan di lakukan di RS Dr Moewardi Surakarta dengan pendekatan quantitative retrospective case control study. Data diambil dari rekam medis antara tahun 2013-2018. Penelitan ini melibatkan 264 neonatal yang terdiri dari 88 kelompok kasus dan 176 kelompok control. Kelompok kasus adalah bayi dengan diagnosa asfiksia yang dilakukan analisis terhadap faktor risiko fetal, sedangkan bayi yang tidak mengalami asfiksia dijadikan kelompok kontrol. Hasil analisis statistik uji Chi-Square dan Fisher Exact ditemukan bahwa kelahiran prematur (OR 2,07 CI 95% P 0,02), persalinan dengan tindakan (OR 3,61 CI 95% P 0,00), berat bayi (OR 2,85 CI 95% P 0,00), posisi janin (OR 2,37 CI 95% P 0,05), tali pusat ( QR 3,071 CI 95% P 0,01) berisiko terhadap insiden asfiksia perinatal. Air ketuban yang bercampur meconium (OR 1,51 CI 95% P 0,16) tidak memiliki risiko dengan Asfiksia perinatal. Kesimpulan: Risiko terhadap insiden asfiksia perinatal meliputi kelahiran prematur, persalinan dengan tindakan, berat bayi, posisi janin, dan tali pusat.Perinatal asphyxia refers to a lack of oxygen during labor, which has the potential to cause death and disability. WHO estimates 4 million children born with asphyxia each year, in which 1 million dies and 1 million survive with severe neurological sequelae. This study aims to analyze fetal and umbilical risk factors in neonatal asphyxia.This research is a quantitative retrospective case-control study, which was conducted at The Dr. Moewardi hospital, Surakarta. Data was taken from medical records from 2013-2018. The case group was patients diagnosed asphyxia, while those who did not experience asphyxia were treated as a control group. A total of 264 samples, consisting of 88 case group respondents and 176 control group respondents. Statistical analysis Chi- Square and Fisher Exact found that preterm birth (OR 2.07 CI 95% P 0.02), labor with instrument or complication (OR 3.61 CI 95% P 0.00), infant weight (OR 2.85 CI 95% P 0, 00), fetal position (OR 2.37 CI 95% P 0.05), umbilical cord (QR 3.071 CI 95% P 0.01) are at risk for the incidence of perinatal Asphyxia. The amniotic fluid mixed with meconium (OR 1.51 CI 95% P 0.16) has no risk with perinatal asphyxia.The risk factors of incidences of perinatal asphyxia were preterm birth, labor with instrument or complication, baby weight, fetal position and umbilical cord.
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Ment, Laura R., William B. Stewart, Charles C. Duncan, and Bruce R. Pitt. "Beagle puppy model of perinatal cerebral insults." Journal of Neurosurgery 65, no. 6 (December 1986): 847–50. http://dx.doi.org/10.3171/jns.1986.65.6.0847.

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✓ Asphyxia, with its attendant hypoxemia, is by far the most common cause of neonatal cerebral infarction, and frequently results in lesions of the parieto-occipital white matter in addition to other neuropathological changes. This study examines the effects of hypoxemia on regional cerebral blood flow (CBF) in the newborn beagle pup. The animals were anesthetized, underwent a tracheotomy, and were paralyzed. Pups were randomly divided into two groups: one group was subjected to hypoxemia produced by altering the oxygen concentration in the inspired air, and the other received no insult. In the hypoxemic pups, the pO2 was 13.1 ± 2.1 mm Hg (mean ± standard deviation). Autoradiographic determinations of CBF were performed by the carbon-14-iodoantipyrine technique 15 minutes after randomization. Significant increases in CBF were found throughout the brains of the hypoxemic pups. The CBF was increased to cortical and central gray regions and to frontal and temporal white matter but was unchanged in the parietal white matter, one of the classic sites of radiological and neuropathological injury in neonates with perinatal asphyxia. An unexpected finding was the increased incidence of germinal matrix and/or intraventricular hemorrhages in the hypoxemic pups.
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Dissertations / Theses on the topic "Asphyxia in the air"

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Yudkin, Patricia L. N. "Consequences of birth asphyxia." Thesis, University of Oxford, 1993. http://ora.ox.ac.uk/objects/uuid:d1bc3e23-8a51-4c7b-a0cd-e76f7b5aaa89.

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To investigate the relationship between birth asphyxia and neurological impairment a cohort of 184 infants with a low (≤3) one-minute Apgar score was studied. All were singletons, apparently normally formed, and born at term (≥37 weeks' gestation) in the John Radcliffe Hospital, between January 1984 and September 1985. The 181 cohort survivors were traced at the age of five years; 159 were assessed by a paediatrician on a battery of neurodevelopmental tests, and information about a further eight was obtained from other sources. Three infants in the cohort died neonatally with a diagnosis of birth asphyxia, and three had spastic quadriplegia, profound developmental delay and visual impairment. Examination of the perinatal histories of these six children, including their fetal heart rate patterns in labour and acid-base status at delivery, found convincing evidence of birth asphyxia. Only one other child in the cohort exhibited similar signs of birth asphyxia; he was unimpaired at the age of five. To assess the impact of birth asphyxia on the overall rate of cerebral palsy, all cases of cerebral palsy born to Oxford residents in the study period were identified. Of 30 cases of cerebral palsy, the three identified in the follow-up study were the only ones whose impairment could be attributed to birth asphyxia in a full-term birth. Birth asphyxia therefore accounted for 10% of all cases of cerebral palsy, a fraction that agrees with previous estimates. The frequency of cerebral palsy due to birth asphyxia was estimated as 1 in 3800 full-term livebirths. A detailed analysis of the test scores of the 159 children assessed by the paediatrician failed to show any association between their acid-base values at delivery and test scores, or between their fetal heart rate patterns in labour and test scores. These results conform with the view that birth asphyxia has an "all or nothing" effect, and that it presents as a cluster of abnormal neonatal signs, including persistent cerebral depression, severe acidaemia, neonatal encephalopathy, and multiorgan dysfunction.
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Power, David John Donovan. "Asphyxia neonatorum in a developing world situation : a study of the impact of asphyxia neonatorum in term infants on the pattern of handicap in the Ciskei; an evalution of its epidemiology and a trial of the efficacy of current therapy." Doctoral thesis, University of Cape Town, 1988. http://hdl.handle.net/11427/27190.

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This study addresses the problem of asphyxia neonatorum in a developing African community in the Mdantsane region of Ciskei. It also documents asphyxia as a prominent cause of childhood handicap, examines aspects of its epidemiology and evaluates the effectiveness of a regimen of phenobarbitone and dexamethasone in limiting subsequent neurological deficit in asphyxiated neonates. Analysis of neonatal deaths at Cecilia Makiwane Hospital over an 18-month period showed that asphyxia accounted for one third of all neonatal deaths. In particular, asphyxia caused two thirds of deaths in infants over 2 Kg birth weight. From a hospital register of handicapped children, 211 had cerebral palsy. Asphyxia was the cause of cerebral palsy in 33% of these children. Spastic quadriplegia, the type of cerebral palsy most often resulting from the cerebral damage associated with asphyxial hypoxic-ischaemic insults, was by far the largest diagnostic category (57%). Asphyxia therefore appears to be the single largest cause of significant handicap in Ciskei. In view of the underdeveloped support services to parents in most developing areas, the problem of asphyxia is of considerable importance. In the study of the epidemiology of asphyxia, details of pregnancy and labour were obtained for 163 asphyxiated term infants and 2758 non- asphyxiated term infants whose mothers had delivered in the hospital. The factors positively associated with asphyxia were: low gravidity and parity, failure to book for antenatal care, the occurrence of antenatal disorders, the occurrence of fetal distress, a prolonged first stage of labour and delivery by caesarean section or vacuum extraction. Maternal age and the actual number of antenatal visits were not associated with asphyxia. The causes of asphyxia assigned by the specialist obstetrician in charge were cephalopelvic disproportion (CPD) (39%), utero-placental pathologies (22%), other (8%), and "unknown" where he could find no abnormality in pregnancy and labour (27%). From these findings it appears that the steps that need to be taken for prevention include: active recruitment of patients to book for antenatal care, more active detection and management of cephalopelvic disproportion and basic research to elucidate the causes of the "unknown" group whom it is speculated have undetected utero-placental pathology.
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Haan, Harmen Hendrik de. "Fetal asphyxia a study in preterm lambs /." Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1994. http://arno.unimaas.nl/show.cgi?fid=6746.

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Лобода, Андрій Миколайович, Андрей Николаевич Лобода, and Andrii Mykolaiovych Loboda. "Forecasting of kidney damage in neonates with asphyxia." Thesis, Lithuanian University of Health Sciences, 2019. http://essuir.sumdu.edu.ua/handle/123456789/72507.

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Більшість показників акушерського анамнезу показали високу прогностичну інформативність (3.0≥І(хі)≥1.0) і можуть відігравати роль факторів ризику пошкодження нирок у новонароджених із асфіксією. Три ознаки мали високий рівень: дистрес плода (І(хі)=2.19), загроза переривання вагітності (І(хі)=1.77) і обвиття пуповини навколо шиї (І(хі)=1.75). Помірне прогностичне значення характерне для інфекцій сечовидільного тракту у матері під час вагітності (1,0>І(хі)≥0,50). Серед неонатальних показників найвищий інформативний рівень продемонстровано для респіраторного дистрес-синдрому (I(хі)=6.71). Висока інформативність була пов'язана з низькою оцінкою за шкалою Апгар на 1-ій (І(хі)=4,36) і 5-й хвилинах (І(хі)=3,62), з чоловічою статтю (І(хі)=1,82), периферійними набряками (I(хі)=1.55) та набряком мозку (I(хі)=1.10). Пошкодження нирок також пов'язане з: низьким рН крові <7,25 (I(хі)=3.00), зниженим парціальним тиском кисню в крові <50 мм рт.ст. (I(хі)=7.06), сироватковим рівнем нейрон-специфічної енолази> 56,2 нг/мл (I(хі)=8,17), цистатином С сироватки> 2600 нг/мл (I(хі)=8,63), сечовим IL-18> 25 пг/мл (I(хі)=1,76), сироватковим IL-6> 35 пг/мл (I(хі)=4,13), сироватковим TNFα> 8,5 пг/мл (I(хі)=7,21), сироватковим IL-10> 10 пг/мл (I(хі)=7,25), сироватковою гамма-глутаміл транспептидазою (GGT)> 120 нмоль/л (I(хі)=4,08) сечовим рівнем ГГТ>47 нмоль/(сек*л) (I(хі)=2,20), а також сироватковим К>4,5 ммоль/л (I(хі)=2,68), сечовим Ca> 0,8 ммоль/л (I(хі)=5.69), сироватковим Pb> 0.200 ммоль/л (I(хі)=7.08).
Большинство показателей акушерского анамнеза показали высокую прогностическую информативность (3.0≥І(хі)≥1.0) и могут играть роль факторов риска повреждения почек у новорожденных с асфиксией. Три признака имели высокий уровень: дистресс плода (І(хі)=2.19), угроза прерывания беременности (І(хі)=1.77) и обвитие пуповины вокруг шеи (І (хі)=1,75). Умеренная прогностическая значимость (1,0<І(хі)≥0,50) была характерна для инфекций мочеиспускательного тракта у матери во время беременности. Среди неонатальных показателей респираторный дистресс продемонстрировал самый высокий уровень информативности (I(хі)=6,71). Высокая информативность ассоциировалась с низким уровнем оценки по Апгар на 1-й (I(хі)=4,36) и 5-й минуте (I(хі)=3,62), с мужским полом (I(хі)=1,82), периферическими отеками (I(хі)=1,55) или отеком мозга (I(хі)=1,10). Поражение почек также связано с: низким рН крови <7,25 (I(хі)=3,00), сниженным парциальным давлением кислорода в крови <50 мм рт. ст. (I(хі)=7,06), уровнем сывороточной нейрон-специфической энолазы> 56,2 нг/мл (I(хі)=8,17), цистатином С сыворотки > 2600 нг/мл (I(хі)=8,63), IL-18 в моче> 25 пг/мл (I(хі)=1,76), сывороточным IL-6> 35 пг/мл (I(хі)=4,13), сывороточным TNFα> 8,5 пг/мл (I(хі)=7,21), сывороточным IL-10>10 пг/мл (I(хі)=7,25), сывороточной гамма-глутамилтранспептидазой (ГГТ)> 120 нмоль/л (I(хі)=4,08), ГГТ в моче> 47 нмоль/(сек*л) (I(хі)=2,20), а также сывороточным К> 4,5 ммоль/л (I(хі)=2,68), Ca в моче> 0,8 ммоль/л (I(хі)=5,69), Pb в сыворотке> 0,200 ммоль/л (I(хі) = 7,08).
Most indicators of obstetric anamnesis showed a high predictive informativeness (3.0≥І(хі)≥1.0) and may play role as risk factors of kidney damage in newborns with asphyxia. The three signs had the high level: the fetal distress (І(хі)=2.19), the threat of abortion (І(хі)= 1.77) and entanglement an umbilical cord around the neck (І(хі)= 1.75). Moderate predictive significance (1,0> І(хі) ≥0,50) was typical for urinary tract infections in the mother during pregnancy. Among the neonatal indicators, respiratory distress demonstrated the highest informative level (I(хі)= 6.71). High informativeness was associated with a low Apgar score on the 1st (I(хі)= 4.36) and the 5th minute (I(хі)= 3.62), with male gender (I(хі)= 1.82), peripheral (I(хі)= 1.55) or brain edema (I(хі)= 1.10). Kidney damage is also associated with: low blood pH <7.25 (I(хі)= 3.00), reduced partial pressure of oxygen in blood <50 mm Hg (I(хі)= 7.06), serum neuron- specific enolase >56.2 ng/ml (I(хі)= 8.17), serum cystatin C>2600 ng/ml (I(хі)= 8.63), urinary IL-18 >25 pg/ml (I(хі)= 1.76), serum IL-6>35 pg/ml (I(хі)= 4.13), serum TNFα>8.5 pg/ml (I(хі)= 7.21), serum IL-10>10 pg/ml (I(хі)= 7.25), serum gamma-glutamyl transpeptidase (GGT)>120 nm/l (I(хі)= 4.08) urinary GGT> 47 nmol/(sec*l) (I(хі)= 2.20), as well as serum K>4.5 mmol/l (I(хі)= 2.68), urinary Ca> 0.8 mmol/l (I(хі)= 5.69), serum Pb>0.200 mmol/l (I(хі)= 7.08).
This study was performed with financial support from the Sumy State University.
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Nguyen, Quyen. "Quantitative diffusion weighted imaging : techniques and applications to perinatal asphyxia." Thesis, University College London (University of London), 2001. http://discovery.ucl.ac.uk/1382401/.

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This thesis describes the results of a study to investigate early cerebral changes in a piglet model of perinatal asphyxia using quantitative diffusion-weighted imaging (DWI) and subsequent work to develop a robust DWI technique to enable similar studies to be performed in neonates. 31Phophorus magnetic resonance spectroscopy and quantitative diffusion and T2 imaging of the cerebrum were performed in a piglet model of perinatal asphyxia. A significant decline in the ratio of phosphocreatine to inorganic phosphate concentrations ([PCr]/[Pi]) was observed during the 48 hours following the transient hypoxicischaemic (H-I) insult. The global directionally averaged apparent diffusion coefficient (ADCav) also declined significantly during the same period and a strong correlation between the [PCr]/[Pi] and ADCav was found. Strong regional and temporal variations in the cerebral response were observed following the H-I insult. In the basal ganglia and parasagittal cortex, significant decline in ADCs was seen approximately 8 hours after the H-I insult. In the thalamus, internal capsule, periventricular white matter and medial cortex, significant ADCs decline was not observed until 32 hours following the H-I insult. A significant T2 increase was observed in the internal capsule but not in the other regions of interest. To enable clinical DWI to be performed in neonates a novel `reacquisition' technique that overcomes the problem of motion artefact in DWI is presented. The reacquisition technique involves the automatic detection and reacquisition of motion-corrupted data in real-time. Computer simulations were used to demonstrate that motion-corrupted data may be detected accurately and reacquired in a time efficient manner. The reacquisition technique was implemented on a Bruker AVANCE scanner in combination with a spinecho 2DFT DWI sequence and an interleaved EPI DWI sequence. The effectiveness of the technique was demonstrated with both a computer-controlled motion phantom and neonates from an ongoing study of perinatal asphyxia.
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Ellis, Matthew Edward. "The public health importance of birth asphyxia in Kathmandu, Nepal." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341882.

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Chandrasekaran, M. "Cerebral magnetic resonance spectroscopy biomarkers and outcome in perinatal asphyxia." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1387843/.

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Background: Neonatal encephalopathy is a common clinical condition affecting 2-3 per 1,000 neonates in the developed world. 10-15% of cases will die in the neonatal period. Therapeutic hypothermia has become the standard of care in the developed world for infants with moderate to severe neonatal encephalopathy only recently, after 2 decades of experimental and clinical studies. Approximately half the infants who receive therapeutic hypothermia still have an abnormal outcome. Research is now being focused on pre-clinical and Phase II clinical studies of drugs, which act synergistically or additively with therapeutic hypothermia. Magnetic resonance spectroscopy (MRS) techniques provide translational biomarkers, which may be used to speed up the development of safe and effective neuroprotective interventions. The precise relation between MRS and brain histology is unknown and it is unclear whether cooling itself alters the prognostic efficacy of MRS. Aim: (i) To explore the relation between MRS biomarkers and the degree of brain pathology observed in our pre-clinical piglet model of perinatal asphyxia; (ii) To assess the predictive value of MRS biomarkers in infants with neonatal encephalopathy Methods: In our piglet study, data from 2 large piglet asphyxia studies investigating neuroprotective agents were analysed. 1. The first was a study of Xenon-augmented hypothermia. Following transient hypoxia-ischemia, 36 piglets were randomised into 4 groups (each n=9), with intervention from 2-26 h: Group (i) normothermia (38.5oC); Group (ii) normothermia (38.5oC) + 24 h 50% inhaled xenon; Group (iii) 24 h therapeutic hypothermia (rectal temperature (Trectal) 33.5oC) or Group (iv) 24 h 50% inhaled xenon +24 h therapeutic hypothermia (Trectal 33.5oC). 2. The second was a study investigating Amiloride as a neuroprotective agent. Following transient hypoxia-ischemia, 18 male piglets (<24 h of age) were randomized to 2 groups (each n=9) (1) normothermia; or (2) 2.5mg/kg of methyl isobutyl amiloride (MIA) at 10 minutes after resuscitation and 8 hourly thereafter. Both studies were performed on a Bruker 4.7 Tesla MR system. Following resuscitation after hypoxia-ischemia, proton (1H) magnetic resonance (MR) spectra were acquired with repetition time (TR) 5 sec, 128 summed transients, and echo times (TE) 25 ms, 144 ms, and 288 ms. (we measured the following peak area ratios: Lactate/N acetyl aspartate (Lac/NAA) and Lactate/Creatine (Lac/Cr) in both white matter and thalamus). Phosphorus (31P) MR spectra were acquired from whole brain using single-pulse acquire with TR 10 s (we measured inorganic phosphate (Pi)/exchangeable phosphate pool (EPP = Pi + PCr + (2γ +β)-NTP), NTP/EPP). Immunohistochemistry was performed on brain sections for activated Caspase 3, TUNEL positive cells and Iba I (activated microglia) to quantify cell death and microglial activation. For the clinical study, we assessed 45 infants (median gestational age – 40 weeks) with moderate to severe neonatal encephalopathy admitted over a 3 year period to the neonatal unit at UCH. Their neurodevelopmental outcome was assessed at 18 months. Results: (i) Experimental Study - Early Biomarkers Early biomarkers (acquired between 2 and 4 hours after hypoxia-ischemia) in particular thalamic Lac/NAA, predicted the 1H MRS area under the curve values from 0-48h and quantitative immunohistochemistry at 48 hours. Late Biomarkers: WM Lac/Cr at 40-48h after HI demonstrated the highest positive correlation with Tunel positive cell death (R20.98, p = 0.01) and NTP/EPP with microglial ramification (R20.68, p = 0.006); this correlation was present in both treated and untreated piglets. (ii) In the clinical study, deep gray matter Lac/NAA was the most accurate predictor of long term adverse neurological outcome following NE; importantly the predictive accuracy of Lac/NAA was unaltered by preceding therapeutic hypothermia. Conclusions: (i) Early thalamic Lac/NAA predicted the subsequent trajectory of energy disruption; this has importance in understanding the relevance of very early MRS studies in babies. White matter lactate/Cr at 40-48h correlated best with quantitative immunohistochemistry (especially TUNEL positive cells) and this relationship was present with and without preceding therapeutic intervention. (ii) In babies with neonatal encephalopathy, the predictive accuracy of Lac/NAA was unaltered by therapeutic hypothermia.
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Cardona, Rocha Federico. "Study of heart rate variability as a marker of asphyxia/hypoxia." Thesis, University of Leicester, 2011. http://hdl.handle.net/2381/9570.

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The onset of labour represents the starting point of a perilous challenge in life, as a new born must adapt to an unknown environment. During this adaptation there are several risks: hypoxia, asphyxia, trauma, intervention and, in worst case scenario, death. These risks can be reduced trough electronic fetal monitoring. During this delicate period the study and analysis of the variability in beat-to-beat intervals of fetal heart rate plays a fundamental role in the pursuit of fetal wellbeing, reduction of fetal morbidity and mortality. Given that the use of an animal model allows direct experimental manipulation of the subjects and their environment and considering the ethical issues and difficulties to acquire data related to asphyxia during labour and delivery, linear techniques (time domain and frequency domain) and non-linear techniques (detrended fluctuation analysis, complexity analysis and Poincarè indices and plots) have been initially implemented for the study of heart rate variability (HRV) using data from the animal model. Data was acquired from experiments in which rats were submitted to controlled episodes of asphyxia (0, 1, 3, 5 and 7 min). Linear and non-linear methods highlighted significant differences in HRV before, during and after the insult. We show how, through a multiparametric analysis, it is possible to detect the onset of asphyxia. Furthermore, tracking the changes in heart rate variability along time, we suggest a novel non-invasive way to assess the amount of injury suffered. With this background we applied HRV analysis to data collected during labour and delivery. We have obtained fetal beat-to-beat heart intervals from non-invasive Doppler ultrasound using Wavelet transform, Hilbert-Huang transform and Autocorrelation function, and these were compared with beat to beat heart intervals extracted from invasive scalp fetal ECG used as a gold standard. For the autocorrelation approach the results of HRV obtained from Doppler ultrasound, using both linear and non-linear analysis, correlate very well with those obtained using fetal scalp ECG. We also modelled and measured the recovery time (from nadir to baseline) following a deceleration of fetal heart rate to study the recovery behaviour and its relation with the development of hypoxic scenarios. The results presented here provide a framework to detect and assess asphyxia by means of linear and non-linear techniques. These techniques have been tested first in an animal model and later in data collected during labour and delivery, showing that Doppler ultrasound provides a reliable alternative for assessing fetal heart rate variations non-invasively during pregnancy and delivery, when fetal scalp ECG is not available. Nevertheless more data needs to be collected and studied using the multiparametric HRV analysis described here to fully validate this approach.
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Koliubakina, L. V., О. V. Vlasova, O. K. Кoloskova, and Т. Y. Мatsei. "Clinical and Diagnostic aspects of developing post-asphyxia syndrome in newborn." Thesis, XVI International Congress of Medical Sciences, Sofia, Bulgaria11-14 MAY 20I7, Вook of abstracts/, 2017. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/12972.

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Hoque, Nicholas Nadir. "Selective head cooling for perinatal asphyxia: effects on physiology and brain injury." Thesis, University of Bristol, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.654564.

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Perinatal asphyxia remains a major cause of morbidity and mortality throughout the world. Despite improvements in obstetric and neonatal care there has been little improvement in rates of death and disability. Therapeutic hypothermia has recently been shown to be the only effective treatment following perinatal asphyxia. Selective Head Cooling (SHe) and Whole Body Cooling (WBe) are methods of applying therapeutic hypothermia. Yet the optimum method of cooling for maximum neuroprotection and minimum adverse effects remains unclear. We retrospectively compared four methods of cooling newborns following perinatal asphyxia. One method of SHC and three methods of WBC, using water-filled gloves, a coolant- filled mattress, and a water- filled body wrap. All methods maintained rectal t emperature within narrow target range. We found that WBC using a servo- controlled system minimised initial over-cooling and reduced subsequent fluctuation in rectal t emperature compared with manually-controlled WBC or SHe. We found similar variation in rectal temperature, heart rate, and mean arterial blood pressure using SHC and manually controlled WBe. We developed a technique of applying SHC with minimal systemic hypothermia as a t reatment for perinatal asphyxia in our established experimental model. We conducted a study to assess the neuroprotective and physiological effects of our technique compared to standard care under normothermic conditions. We did not find any difference in brain injury between treatment groups but increased mortality in the hypothermia group. We have.previously used a neuropathology score in our established model of perinatal asphyxia in order to assess treatment effects. Our neuropathology score incorporates subjective assessments of area injure'd and morphological cellular changes in several brain regions. We conducted quantitative cell counting to assess brain injury following perinatal asphyxia. Cell count correlated with neuropathology score in the putamen and hippocampus CA1 and we were able to validate our neuropathology score to assess outcome.
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Books on the topic "Asphyxia in the air"

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Council, National Safety, ed. Instructor's resource manual for CPR, 1992 guidelines. Boston: Jones and Bartlett Publishers, 1993.

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Council, National Safety, ed. Instructor's resource manual for CPR. 2nd ed. Sudbury, MA: Jones and Bartlett Publishers, 1997.

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Haddad, Joseph, and Elie Saliba, eds. Perinatal Asphyxia. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77896-4.

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Lacoius-Petruccelli, Alberto. Perinatal Asphyxia. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-1807-1.

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Perinatal asphyxia. New York: Plenum Medical Book Co., 1986.

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J, Haddad, Saliba E. 1950-, and Arbeille Ph, eds. Perinatal asphyxia. Berlin: Springer-Verlag, 1993.

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Sabaratnam, Arulkumaran, and Jenkins H. M. L, eds. Perinatal asphyxia. London: Sangam, 2000.

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Feio, Candice Carvalho. Asfixia: Asphyxia NY. São Paulo: Fotô Editorial, 2021.

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Dev, Maulik, ed. Asphyxia and fetal brain damage. New York: Wiley-Liss, 1998.

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Lectures on anesthetics and on asphyxia. [Park Ridge, Ill: Wood Library-Museum, 1989.

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Book chapters on the topic "Asphyxia in the air"

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Wood, J. A. "The respiratory system and asphyxia." In The Theory of Advanced First Aid, 17–36. Dordrecht: Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-017-3513-1_3.

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Wood, J. A. "The respiratory system and asphyxia." In The Theory of Advanced First Aid, 17–36. Dordrecht: Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-009-4908-9_3.

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Prosje, Michelle A. "Asphyxia." In Encyclopedia of Child Behavior and Development, 148–51. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-0-387-79061-9_201.

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Lacoius-Petruccelli, Alberto. "Asphyxia." In Perinatal Asphyxia, 11–15. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-1807-1_1.

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Genet, Pia, and Coraline Egger. "Asphyxia." In Forensic Imaging, 99–109. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-83352-7_8.

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DiMaio, Vincent J. M., and D. Kimberley Molina. "Asphyxia." In DiMaio's Forensic Pathology, 233–78. 3rd ed. Boca Raton: CRC Press, 2021. http://dx.doi.org/10.4324/9780429318764-8.

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Dettmeyer, Reinhard B., Marcel A. Verhoff, and Harald F. Schütz. "Asphyxia." In Forensic Medicine, 227–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-38818-7_14.

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Merck, Melinda D., and Doris M. Miller. "Asphyxia." In Veterinary Forensics: Animal Cruelty Investigations, 169–84. West Sussex, UK: John Wiley & Sons, Inc.,, 2013. http://dx.doi.org/10.1002/9781118704738.ch9.

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Cioffi, William G., Michael D. Connolly, Charles A. Adams, Mechem C. Crawford, Aaron Richman, William H. Shoff, Catherine T. Shoff, et al. "Traumatic Asphyxia." In Encyclopedia of Intensive Care Medicine, 2295–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_525.

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Kawase, Koya, and Osuke Iwata. "Birth Asphyxia." In Cerebral Palsy, 245–51. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-2217-6_26.

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Conference papers on the topic "Asphyxia in the air"

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Widiyaningrum, Alfiati Nanda, Bhisma Murti, and Eti Poncorini Pamungkasari. "Effect of Meconium Stained Amniotic Fluid on The Risk of Infants Asphyxia: A Meta-Analysis." In The 7th International Conference on Public Health 2020. Masters Program in Public Health, Universitas Sebelas Maret, 2020. http://dx.doi.org/10.26911/the7thicph.03.130.

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ABSTRACT Background: Meconium aspiration syndrome refers to the aspiration of meconium and amniotic fluid by the fetus. It can occur when the fetus is still in the uterus, passing through the birth canal or when it takes its first breath after birth. Meconium aspiration is a serious condition with high morbidity and mortality. This study aimed to examine the effect of meconium stained amniotic fluid on the risk of infants asphyxia. Subjects and Method: Meta analysis and systematic review was conducted by collecting published articles from PubMed, Google Scholar, Clinical Key, Science Direct, and Springer Link databases. Keywords used risk factor, asphyxia, birth asphyxia, meconium stained amniotic, meconium stained liquor, and cross sectional. The inclusion criteria were full text, using English language, using cross-sectional study design, and reporting adjusted odds ratio. The study population was infants. Intervention was meconium stained amniotic liquid with comparison clean amniotic liquid. The study outcome was asphyxia. The collected articles were selected by PRISMA flow chart. The quantitative data were analyzed by fixed effect model using Revman 5.3. Results: 7 studies from Ethiopia reported that meconium stained amniotic fluid increased the risk of asphyxia in infants 5.83 (aOR= 5.83; CI 95%= 4.15 to 8.20; p <0.001). Conclusion: Meconium stained amniotic fluid increases the risk of asphyxia in infants. Keywords: meconium, amniotic fluid, asphyxia, infants Correspondence: Alfiati Nanda Widiyaningrum. Masters Program in Public Health, Universitas Sebelas Maret. Jl. Ir. Sutami 36A, Surakarta 57126, Central Java. Email: widiyaningruma@gmail.com. Mobile:081327524537. DOI: https://doi.org/10.26911/the7thicph.03.130
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Cedrone, K. D., C. Mielcarz, K. R. Olson, and S. Data. "Augmented infant resuscitation (air) device to improve management of intrapartum related deaths (“birth asphyxia”)." In Appropriate Healthcare Technologies for Low Resource Settings (AHT 2014). Institution of Engineering and Technology, 2014. http://dx.doi.org/10.1049/cp.2014.0786.

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Chen, Lanzhen. "Research on a New Spot-first-aid of Foreign Body Asphyxia Hypopharynx." In Advanced Science and Technology 2016. Science & Engineering Research Support soCiety, 2016. http://dx.doi.org/10.14257/astl.2016.121.42.

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Zabidi, A., L. Y. Khuan, and W. Mansor. "Asphyxia screening kit." In 2012 34th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2012. http://dx.doi.org/10.1109/embc.2012.6346175.

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Yunita, Laurensia, Fadhiyah Noor Annisa, and Sundari Sundari. "Effect of Childbirth Complications Occurrence Of Asphyxia Neonatorum." In 2nd Sari Mulia International Conference on Health and Sciences 2017 (SMICHS 2017) � One Health to Address the Problem of Tropical Infectious Diseases in Indonesia. Paris, France: Atlantis Press, 2017. http://dx.doi.org/10.2991/smichs-17.2017.73.

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Calabrese, Clementina, Alessandra Marinari, Lucia Taurino, Alessandra Catucci, Lorenza Chiossi, Salvatore Cringoli, Francesca Lotti, et al. "P114 Also adipose tissue pays consequencies of perinatal asphyxia." In 8th Europaediatrics Congress jointly held with, The 13th National Congress of Romanian Pediatrics Society, 7–10 June 2017, Palace of Parliament, Romania, Paediatrics building bridges across Europe. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2017. http://dx.doi.org/10.1136/archdischild-2017-313273.202.

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Syamsi, Efrida Yusriyanti, and Nuli Nuryanti Zulala. "Premature Rupture of Membrane (PROM) Increasing Asphyxia Neonatorum Risk." In International Conference on Health and Medical Sciences (AHMS 2020). Paris, France: Atlantis Press, 2021. http://dx.doi.org/10.2991/ahsr.k.210127.053.

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Silva, Barbara, Maria Ribeiro, and Teresa S. Henriques. "Compression of Different Time Series Representations in Asphyxia Detection." In 2022 E-Health and Bioengineering Conference (EHB). IEEE, 2022. http://dx.doi.org/10.1109/ehb55594.2022.9991468.

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Onu, Charles C., Jonathan Lebensold, William L. Hamilton, and Doina Precup. "Neural Transfer Learning for Cry-Based Diagnosis of Perinatal Asphyxia." In Interspeech 2019. ISCA: ISCA, 2019. http://dx.doi.org/10.21437/interspeech.2019-2340.

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Abry, P., H. Helgason, P. Goncalves, E. Pereira, P. Gaucherand, and M. Doret. "Multifractal analysis of ECG for intrapartum diagnosis of fetal asphyxia." In 2010 IEEE International Conference on Acoustics, Speech and Signal Processing, ICASSP 2010. IEEE, 2010. http://dx.doi.org/10.1109/icassp.2010.5495583.

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Reports on the topic "Asphyxia in the air"

1

McAllister, Branford J. Air-to-Air Continuation Training in the Tactical Air Command. Fort Belvoir, VA: Defense Technical Information Center, April 1985. http://dx.doi.org/10.21236/ada157151.

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Uzzell, David R. Air-to-Air Force's Doctrine and Training for an Air Occupation. Fort Belvoir, VA: Defense Technical Information Center, March 1997. http://dx.doi.org/10.21236/ada388266.

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Patton, G. W. Air surveillance. Office of Scientific and Technical Information (OSTI), June 1995. http://dx.doi.org/10.2172/433030.

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4

CORPS OF ENGINEERS WASHINGTON DC. Air Stripping. Fort Belvoir, VA: Defense Technical Information Center, October 2001. http://dx.doi.org/10.21236/ada402975.

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Sherman, William C. Air Warfare. Fort Belvoir, VA: Defense Technical Information Center, March 2002. http://dx.doi.org/10.21236/ada421698.

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Egyed, M., P. Blagden, D. Plummer, P. Makar, C. Matz, M. Flannigan, M. MacNeill, et al. Air quality. Natural Resources Canada/CMSS/Information Management, 2022. http://dx.doi.org/10.4095/329531.

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Litka, A. F., and F. E. Becker. Air-cooled CWS warm air furnace. Final report. Office of Scientific and Technical Information (OSTI), August 1995. http://dx.doi.org/10.2172/132656.

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Wetter, Michael. Simulation model air-to-air plate heat exchanger. Office of Scientific and Technical Information (OSTI), January 1999. http://dx.doi.org/10.2172/7352.

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Robinson, James K. Air Expeditionary Force: The Air Forces' New Capability. Fort Belvoir, VA: Defense Technical Information Center, April 1999. http://dx.doi.org/10.21236/ada364124.

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Heilenday, Frank. Principles of Air Defense and Air Vehicle Penetration. Fort Belvoir, VA: Defense Technical Information Center, March 2000. http://dx.doi.org/10.21236/ada375233.

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