Laman Amin-Zaki
University of Baghdad
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Featured researches published by Laman Amin-Zaki.
Journal of Neuropathology and Experimental Neurology | 1978
Ben H. Choi; Lowell W. Lapham; Laman Amin-Zaki; T. Saleem
Detailed clinical and neuropathological studies have been made in two fullterm newborn human infants who were exposed to methylmercury in utero as a result of maternal ingestion of methylmercury-contaminated bread in early phases of pregnancy. High levels of mercury were detected in various regions of the brain at autopsy. Study of the brains revealed a disturbance in the development in both cases, consisting essentially of an incomplete or abnormal migration of neurons to the cerebellar and cerebral cortices, and deranged cortical organization of the cerebrum. There were numerous heterotopic neurons, both isolated and in groups, in the white matter of cerebrum and cerebellum and the laminar cortical pattern of the cerebrum was disturbed in many regions as was shown by the irregular groupings and the deranged alignment of cortical neurons. Prominent in the white matter of the cerebrum and the cerebellum was diffuse gemistocytic astrocytosis accompanied by an accumulation of mercury grains in their cytoplasm. These findings indicate a high degree of vulnerability of human fetal brain to maternal intoxication by methylmercury. A major effect appears to be related to faulty development and not to destructive focal neuronal damage as has been observed in mercury intoxication in adults and children exposed postnatally.
Pediatrics | 1974
Laman Amin-Zaki; Sami Elhassani; Mohamed A. Majeed; Thomas W. Clarkson; Richard A. Doherty; Michael R. Greenwood
A disastrous epidemic of methylmercury poisoning occurred in rural Iraq early in 1972, due to the ingestion of home-made bread prepared from wheat treated with a methylmercury fungicide. We report the clinical and laboratory evaluation of 15 infant-mother pairs exposed to methylmercury during pregnancy, including mercury determinations in blood samples of mothers and infants, and in milk samples from mothers, during the first seven months following the epidemic.
Environmental Research | 1989
Christopher Cox; Thomas W. Clarkson; D. O. Marsh; Laman Amin-Zaki; Sa'adoun Tikriti; Gary G. Myers
A new method of estimating fetal exposure is used in a dose-response analysis of data from the 1971 outbreak of methyl mercury poisoning in rural Iraq. An X-ray fluorescence instrument for the measurement of single strands of human hair was employed to obtain longitudinal profiles recapitulating fetal exposure. Logit and hockey-stick models as well as nonparametric smoothing are used to describe data on delayed development and central nervous system abnormality.
BMJ | 1978
Laman Amin-Zaki; M A Majeed; T W Clarkson; M R Greenwood
The clinical features of 49 children who had eaten bread contaminated with methylmercury in rural Iraq were reviewed. Symptoms and signs relating to the nervous system--varying degrees of ataxia, weakness, and visual and sensory changes--dominated the clinical picture. The severity of poisoning was related to the blood mercury concentration, as was the degree of recovery. Follow-up over two years showed that children who had had mild or moderate poisoning slowly but steadily improved, some of them recovering normal function, though all had a residual generalized hyperreflexia. In some patients ataxia and motor weakness disappeared. Visual changes also improved, though less completely, and of 17 blind children, only five had recovered partial sight by the end of two years. Seven of the 18 children who suffered very severe poisoning were left physically and mentally incapacitated. The degree of clinical progress shown by these children was better than that shown by some other groups of patients, possibly because the poisoning was relatively acute and mercury consumption was stopped immediately after its effects had become obvious.
Clinical Toxicology | 1981
D. O. Marsh; Gary J. Myers; Thomas W. Clarkson; Laman Amin-Zaki; S. Tkriti; M. A. Majeed; A. R. Dabbagh
Eighty-four Iraqi mothers and their infants had been exposed to methylmercury during pregnancy. The methylmercury had been ingested as a fungicide. Peak maternal hair mercury concentrations were related to the frequency of maternal symptoms during pregnancy and to neurological effects in the infants. These include various degrees of psychomotor retardation. Severe neurological deficits were observed in five children whose maternal peak hair mercury concentrations were 165 to 320 ppm. Minimal symptoms were reported for mothers and children when peak maternal hair levels were below 68 ppm. Minimal clinical neurological signs occurred in children when peak maternal hair mercury concentrations were at an undetermined point between 68 and 180 ppm. Greater fetal risk appears to be associated with exposure during the second trimester. This exposure to methylmercury was acute and the results may not be extrapolated to a constant level of exposure throughout pregnancy. The effects of fetal exposure to methylmercury in marine fish may differ.
Environmental Research | 1978
Michael R. Greenwood; Thomas W. Clarkson; Richard A. Doherty; Allen H. Gates; Laman Amin-Zaki; Sami Elhassani; Mohammed A. Majeed
An epidemic of methylmercury poisoning occurred in rural Iraq early in 1972 due to the ingestion of homemade bread prepared from wheat treated with a methylmercury fungicide. We report observations of the blood mercury clearance half-times of lactating women and nonlactating groups who were exposed during the epidemic. Blood clearance half-times calculated by linear regression analysis show that in lactating females, the mean half-time is 42 days and in nonlactating females and males, the mean half-time is 75 days. Experiments in mice also show such differences in whole body half-time: 5.6 days in lactating females and 9.3 days in nonlactating females.
Archive | 1981
Thomas W. Clarkson; Christopher Cox; D. O. Marsh; Gary J. Myers; Sadoun K. Al-Tikriti; Laman Amin-Zaki; Abdul Ruzak Dabbagh
Public concern over the health hazards of methylmercury was aroused by the two outbreaks of poisoning in Japan: in Minamata in the 1950s and in Niigata Prefecture in the 1960s (for details, see reference 26). The cause of the mass poisoning was the consumption of fish that had been contaminated by industrial discharge of methylmercury compounds.
BMJ | 1983
Laman Amin-Zaki
Stephenson JBP. Anoxic seizures or epilepsy ? Br MedJ7 1977;ii:45. ± Gastaut H, Broughton R. Epileptic seizures. Springfield, Illinois: Thomas, 1972. Gastaut H. Syncopes: generalised anoxic cercbral seizures. In: Vinken P1, Bruyn GW, eds. Handbook of clinical neurology. Vol 15. Amsterdam: NorthHolland, 1974:815-35. Stephenson JBP. Febrile convulsions and reflex anoxic seizures. In: Rose FC, ed. Research progress in epilepsy. London: Pitman Medical, 1983:244. Stephenson JBP. Reflex anoxic seizures and ocular compression. Dev Med Child Neurol 1980;22 :380-6.
Science | 1973
F. Bakir; S. F. Damluji; Laman Amin-Zaki; M. Murtadha; A. Khalidi; N. Y. Al-Rawi; S. Tikriti; H. I. Dhahir; Thomas W. Clarkson; J. C. Smith; Richard A. Doherty
JAMA Neurology | 1987
D. O. Marsh; Thomas W. Clarkson; Christopher Cox; Gary J. Myers; Laman Amin-Zaki; Sa'adoun Al-Tikriti