Publications by authors named "Mary O"

3 Publications

  • Page 1 of 1

Maternal age at birth and under-5 mortality in Nigeria.

East Afr J Public Health 2009 Apr;6(1):11-4

Department of Demography & Social Statistics, Obafemi Awolowo University, Ile Ife, Nigeria.

Objective: The paper examined the impact of maternal age at birth on under-5 death in Nigeria.

Method: Secondary data were generated from the 2003 Nigeria Demographic and Health Surveys in examining the relationship between maternal age at birth and under-5 mortality risk. Relationships between variables were tested through bivariate and logistic analyses.

Results: Out of 7620 sampled women for the study, almost 60% were less than 30 years old, the median age was 26 years- a youthful population. Analyses of the data revealed a high under-5 mortality rate (45.4%), a general high home delivery (62.4%) among Nigerian women, which dictates a low rate at which assistance by health professional is being sought during childbirth . Furthermore, mothers' median age at first birth was less than 19, while under-5 death was significantly pronounced among younger (less than 20 years) mothers and older women (above 35 years) (p<0.05). Maternal education which was significantly low among younger mothers was a predictor of under-5 mortality.

Conclusion: Under -5 mortality is still high especially among younger mothers. Thus resolving this challenge in Nigeria will be inadequate if early childbearing issues are not addressed using a tailored framework alongside with the need to improve maternal education in Nigeria.
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http://dx.doi.org/10.4314/eajph.v6i1.45735DOI Listing
April 2009

Role of substantia nigra-amygdala connections in surprise-induced enhancement of attention.

J Neurosci 2006 May;26(22):6077-81

Department of Psychological and Brain Sciences, Johns Hopkins University, Baltimore, Maryland 21218, USA.

Coding of prediction error by midbrain dopamine neurons has been examined extensively in the framework of associative learning theory. Most of this research has focused on the role of prediction error in determining the reinforcement value of unconditioned stimuli: poorly predicted ("surprising") outcomes are more effective reinforcers and produce a greater dopamine response than well predicted outcomes. However, surprise also enhances attention to cues that signal poorly predicted outcomes. Previous reports from our laboratories demonstrated that circuitry, including the amygdala central nucleus (CeA), the cholinergic neurons of the substantia innominata/nucleus basalis region, and their innervation of the posterior parietal cortex, is critical to these surprise-induced enhancements of attention in associative learning. The present study considered the origin of prediction error information important for the operation of this system by examining the effects of disrupting communication between the midbrain substantia nigra pars compacta (SNc) and the CeA. Rats received unilateral lesions of the SNc and lesions of the CeA in either the contralateral or ipsilateral hemisphere. Contralateral lesions eliminated the surprise-induced enhancement of attention and learning that was displayed by rats with ipsilateral control lesions. These results show that SNc-CeA communication is critical to mechanisms by which the coding of prediction error by midbrain dopamine neurons is translated into enhancement of attention and learning modulated by the cholinergic system.
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http://dx.doi.org/10.1523/JNEUROSCI.1316-06.2006DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6675230PMC
May 2006

Cdk5 is a key factor in tau aggregation and tangle formation in vivo.

Neuron 2003 May;38(4):555-65

Center for Dementia Research, Nathan S. Kline Institute, New York University, 140 Old Orangeburg Road, Orangeburg, NY 10962, USA.

Tau aggregation is a common feature of neurodegenerative diseases such as Alzheimer's disease, and hyperphosphorylation of tau has been implicated as a fundamental pathogenic mechanism in this process. To examine the impact of cdk5 in tau aggregation and tangle formation, we crossed transgenic mice overexpressing the cdk5 activator p25, with transgenic mice overexpressing mutant (P301L) human tau. Tau was hyperphosphorylated at several sites in the double transgenics, and there was a highly significant accumulation of aggregated tau in brainstem and cortex. This was accompanied by increased numbers of silver-stained neurofibrillary tangles (NFTs). Insoluble tau was also associated with active GSK. Thus, cdk5 can initiate a major impact on tau pathology progression that probably involves several kinases. Kinase inhibitors may thus be beneficial therapeutically.
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http://dx.doi.org/10.1016/s0896-6273(03)00259-9DOI Listing
May 2003
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