다중혈관 관상동맥 환자에서 y-문합을 이용하여 양쪽 내흉동맥만을 사용한 우회술의 조기 성적

Benjamini and Hochberg suggest that the false discovery rate may be the appropriate error rate to control in many applied multiple testing problems. A simple procedure was given there as an FDR controlling procedure for independent test statistics and was shown to be much more powerful than comparable procedures which control the traditional familywise error rate. We prove that this same procedure also controls the false discovery rate when the test statistics have positive regression dependency on each of the test statistics corresponding to the true null hypotheses. This condition for positive dependency is general enough to cover many problems of practical interest, including the comparisons of many treatments with a single control, multivariate normal test statistics with positive correlation matrix and multivariate $t$. Furthermore, the test statistics may be discrete, and the tested hypotheses composite without posing special difficulties. For all other forms of dependency, a simple conservative modification of the procedure controls the false discovery rate. Thus the range of problems for which a procedure with proven FDR control can be offered is greatly increased.

/pdf/the-control-of-the-false-discovery-rate-in-multiple-testing-426hrdkyhb.pdf

The control of the false discovery rate in multiple testing under dependency

▪ Abstract Socioeconomic status (SES) is one of the most widely studied constructs in the social sciences. Several ways of measuring SES have been proposed, but most include some quantification of family income, parental education, and occupational status. Research shows that SES is associated with a wide array of health, cognitive, and socioemotional outcomes in children, with effects beginning prior to birth and continuing into adulthood. A variety of mechanisms linking SES to child well-being have been proposed, with most involving differences in access to material and social resources or reactions to stress-inducing conditions by both the children themselves and their parents. For children, SES impacts well-being at multiple levels, including both family and neighborhood. Its effects are moderated by children's own characteristics, family characteristics, and external support systems.

Socioeconomic status and child development.

Recent research consistently reports that persistent poverty has more detrimental effects on IQ, school achievement, and socioemotional functioning than transitory poverty, with children experiencing both types of poverty generally doing less well than never-poor children. Higher rates of perinatal complications, reduced access to resources that buffer the negative effects of perinatal complications, increased exposure to lead, and less home-based cognitive stimulation partly account for diminished cognitive functioning in poor children. These factors, along with lower teacher expectancies and poorer academic-readiness skills, also appear to contribute to lower levels of school achievement among poor children. The link between socioeconomic disadvantage and children's socioemotional functioning appears to be mediated partly by harsh, inconsistent parenting and elevated exposure to acute and chronic stressors. The implications of research findings for practice and policy are considered.

Socioeconomic disadvantage and child development

Vulnerable periods during the development of the nervous system are sensitive to environmental insults because they are dependent on the temporal and regional emergence of critical developmental processes (i.e., proliferation, migration, differentiation, synaptogenesis, myelination, and apoptosis). Evidence from numerous sources demonstrates that neural development extends from the embryonic period through adolescence. In general, the sequence of events is comparable among species, although the time scales are considerably different. Developmental exposure of animals or humans to numerous agents (e.g., X-ray irradiation, methylazoxymethanol, ethanol, lead, methyl mercury, or chlorpyrifos) demonstrates that interference with one or more of these developmental processes can lead to developmental neurotoxicity. Different behavioral domains (e.g., sensory, motor, and various cognitive functions) are subserved by different brain areas. Although there are important differences between the rodent and human brain, analogous structures can be identified. Moreover, the ontogeny of specific behaviors can be used to draw inferences regarding the maturation of specific brain structures or neural circuits in rodents and primates, including humans. Furthermore, various clinical disorders in humans (e.g., schizophrenia, dyslexia, epilepsy, and autism) may also be the result of interference with normal ontogeny of developmental processes in the nervous system. Of critical concern is the possibility that developmental exposure to neurotoxicants may result in an acceleration of age-related decline in function. This concern is compounded by the fact that developmental neurotoxicity that results in small effects can have a profound societal impact when amortized across the entire population and across the life span of humans.

Critical periods of vulnerability for the developing nervous system: evidence from humans and animal models.

Maternal urinary-tract infections and fetal leukoencephalopathy.

We sought explanations for African-American mothers' increased risk of chorioamnionitis by sequentially adjusting for confounder variables both individually and in groups. We searched for a subset of covariates that had the most influence on the chorioamnionitis odds ratio (OR) of these women. The sample consisted of 305 African-American and 520 White mothers who gave birth to a very-low-birthweight (< or = 1500 g) infant between 1991 and 1993, whose placenta was examined according to protocol and whose hospital chart was reviewed. Histologically proven chorioamnionitis was present in 43% of the placentas from African-American women and in 27% of those from Whites (crude OR 2.1, 95% confidence interval 1.5, 2.8). Singleton status appeared to be the most important effect modifier, with significant crude ORs of 1.5 among singletons and 3.4 among non-singletons. Using logistic regression models in the whole sample and in subgroups, we sought to 'explain away' this increased risk. Indeed, addition of information about confounder variables resulted in considerable reduction in the ORs to 1.1 among singletons and 1.9 among non-singletons. Particularly important among the confounders were singleton birth, Medicaid insurance, duration of ruptured membranes and gestational age. We discuss the possibility that this set of confounding variables conveys, in part, the same information as the variable African-American, and also perhaps information about the availability and/or utilisation of prenatal health care.

What explains away the increased risk of histological chorioamnionitis in African-American mothers of very-low-birthweight infants?

Lindsten, J. (1973) ‘An explanation of the apparently increased incidence of moderate mental retardation in Turner’s syndrome.’ Behavior Genetics, 3, 37-43. 18. Alexander, D., Money. J. (1966) ‘Turner’s syndrome a n d Gerstman’s syndrome: neurophysiologic comparisons.’ Neuropsychologia, 4, 265-273. 19. Money, J . , Alexander, D. (1966) ‘Turner’s syndrome: further demonstrations of thy presence of specific cognitional deficiencies. Journal of Medical Genetics. 3, 4 7 4 8 . 20. Waber, D . P. (1979) ‘Neurophysiological aspects of Turner’s syndrome.’ Developmental Medicine and Child Neurology. 21, 58-70. 21. Money, J . (1973)‘Turner’s syndrome and parietal lobe functions.’ Cortex, 9, 385-393. 22. Kolb, J . E.. Heaton, R . K . (1975) ‘Lateralized neurologic deficits and psychopathology in a Turner syndrome patient.’ Archives of General Psychiatry, 32, I 1981200. 23. Luria, A. R. (1973) The Working Brain (Trans. B. Haigh). New York: Basic Books. 24. Netley, C. (1976) ‘Dichrotic listening of callosal agenesis and Turner’s syndrome patients.’ In Segalowicz, S. J., Gruber , F. A. (Eds.)Languuge Development and Neurological Theory. New York: Academic Press. 25. Netley, C., Rovet, J. (1982)‘Atypical hemispheric Iateraliiation in Turner syndrome su6jects., Cortex. 18, 377-3x4. 26. Alexander, D., Money, J. (1965) ‘Reading ability, object constancy and Turner’s syndrome.’ Perceptual and Motor Skills. 20, 981-984. 27. Anastasi, A. ( 1958) Differential Psychology: Individual and Group Differences in Behavior. New York: Macmillan. 28. Maccoby, E. E. (1966) ‘Sex differences in intellectual functioning.’ In Maccoby, E. E . (Ed.) The Development of Sex Differences. Palo Alto: Stanford University Press.

To What Extent Does Food Sensitivity Contribute to Headache Recurrence

Unlike maternal phenylketonuria (PKU) which produces severe birth defects when untreated during pregancy, maternal non-PKU mild hyperphenylalaninemia (MHP) has a less severe impact but whether it is benign or may have long-term consequences for offspring has been unclear From an international survey of maternal MHP we obtained information about 86 mothers (blood phenylalanine (Phe) 150–720 µmol/1), their 219 untreated pregnancies and 173 offspring Spontaneous fetal loss and congenital anomalies were no more frequent than normally expected Median Z-scores for birth length and birth head circumference and offspring IQ (100), however, were significantly lower for maternal Phe > 400 µjnol/1 than for maternal Phe <400 µmol/1, in which the median offspring IQ was 108 Data on maternal MHP from the prospective Maternal PKU Collaborative Study (MPKUCS) are as yet incomplete but seem to be conforming to the general pattern of the international survey We conclude that maternal blood Phe levels above 400 µmol/1 in maternal MHP are associated with lower birth measurements and slightly lower offspring IQ It would seem that dietary intervention to lower the maternal Phe levels to below 400 µmol/l might be indicated in maternal MHP pregnancies with the higher blood Phe levels

Maternal non-phenylketonuric mild hyperphenylalaninemia.

We offer the hypothesis that some forms of cerebral white matter damage (WMD) in preterm neonates might be caused by transplacental viral infection of the fetus during the first or second trimester of pregnancy. Potts and colleagues1 speculated on the possible role of a human pestivirus (PV) in the aetiology of congenital microcephaly. We suggest PV might be a candidate virus for some form of WMD. We further offer our view that a virus induced cytokine cascade might place the fetus at double jeopardy—that is, disturb white matter development and lead to preterm birth.

White matter damage is the most important predictor of childhood neuromotor disability among those born preterm. About 50% of infants who have echolucent zones in the periventricular white matter or ventriculomegaly on neonatal cranial ultrasound scans subsequently develop cerebral palsy.2 The multiple expressions of WMD, both on histological examination and neonatal cranial ultrasound scan, as focal, multifocal, or diffuse WMD,3 make multiple aetiologies likely. Some forms of WMD might be related to a hypoxic–ischaemic insult, but others might be associated with infection.

Four types of WMD can be distinguished on the basis of their location, histological patterns, and ultrasonographic appearance.3The first two forms comprise unifocal haemorrhagic infarctions, leading to periventricular echodensities on neonatal cranial ultrasound images, and multifocal necroses, leading to hypoechoic ultrasound images often described as “periventricular leucomalacia” (PVL). Current textbooks focus on fetal or newborn hypoxia–ischaemia as the pathogenesis of focal and multifocal forms of WMD.4 This is supported by studies showing that periventricular white matter damage can be induced by ligating the carotid arteries of mongrel …

https://fn.bmj.com/content/fetalneonatal/78/3/F230.full.pdf

Alan Leviton

Papers

Maternal urinary-tract infections and fetal leukoencephalopathy.

What explains away the increased risk of histological chorioamnionitis in African-American mothers of very-low-birthweight infants?

To What Extent Does Food Sensitivity Contribute to Headache Recurrence

Maternal non-phenylketonuric mild hyperphenylalaninemia.

Is some white matter damage in preterm neonates induced by a human pestivirus