Chaoyun Liang *,Yu-Cheng Liu
Background and Objective: Experienced designers make connections with knowledge stored in their memory and transform their solutions to respond to design problems. However, little research has explained how they engage in this transformation. Methods: The current study examined the brain activation, supplemented with narrative information, resulting from pictorial stimulation among experienced designers while they engaged in tasks that involve transforming imagination.
Results: This study recruited 15 healthy and experienced designers to participate in an electroencephalography experiment and a structured in-depth interview.
Conclusions:The results illuminated several key variations in brain activation, including those that existed (i) among various lobes when the designers engaged in both visual stimulation and design improvement tasks involving transforming imagination; (ii) among the three indicators of transforming imagination in both experimental tasks; and (iii) between the two experimental tasks involving transforming imagination.
Aim: Hippocampus is an important brain structure responsible for learning and episodic memory. It is also a plastic and vulnerable structure damaged by a variety of factors. Incidentally, it is among the first and the most severely affected structure that undergoes atrophy in Alzheimer’s disease (AD), the leading cause of dementia worldwide. Though considered neurodegenerative; the role of vascular and other associated factors causing hippocampal atrophy in AD is under investigation. In the present study; an attempt was made to explore the effect of presence of various clinical and biochemical predictors on the hippocampal volumes in patients with AD.
Methods: We screened 280 subjects coming to the Department of Neurology of a Tertiary Care Hospital with memory/and or cognitive complaints starting from July 2012 to December 2015 and enrolled 144 subjects. Those who met the diagnostic Criteria for the diagnosis of probable AD (National Institute of Neurological and Communicative Disorders and Stroke, Alzheimer’s disease related Disease Association criteria (NINCDS-ARDA), were recruited for the present study. Selected patients were segregated into AD-associated comorbidities or biochemical alterations in AD e.g. AD-diabetes, AD-hypertension, AD-depression, AD-seizures categories or AD-hyperhomocysteinemia, AD-hypercortisolemia, AD-vitamin D3 and AD-vitamin B12 deficient patients groups. Selected patients underwent Magnetic Resonance Imaging of the Brain (MRI Brain) and T1 weighted images in a plane perpendicular to long axis of hippocampus were obtained. Hippocampal volumes were measured manually using a standard protocol. The comparison of hippocampal volumes was done among the groups e.g. with the cognitively normal individuals and those patients of AD with or without vascular and non vascular risk factors.
Results: Out of 280 patients screened, 144 met the diagnostic criteria for AD. A total of 8 patients (n=64) per predictor group were selected in the predictor-stratified group. There was a statistically significant difference between the hippocampal volumes of the cognitively normal elderly (n=30), those patients with AD without vascular or other risk factors (n=20), and patients with cumulative risk factors (n=30) [p-value<0.05]. Hippocampal volumes of those with atleast one of the biochemical/vascular or non vascular risk factor for hippocampal atrophy was compared with the patients without risk factors and there was a statistically significant difference between these groups (p-value<0.05). There was a moderately strong correlation between hippocampal volume and MMSE (Pearson Correlation Coefficient=0.56).
Conclusions: Those with the diagnosis of AD and associated seizures, depression and patients of AD with diabetes and hypertension combined together had statistically significant volume reduction of hippocampus compared to AD patients without risk factors for hippocampal atrophy
Lou de Olivier.
Known as “sufrimiento fetal” in Spanish, “fetal distress” in Great Britain, “anoxia perinatal” in Portuguese language countries, with variation also as “hipoxia ou asfixia neonatal”. All these terms mean absence or decrease of oxygen in the brain during birth. At the time of the first survey the term fetal distress was used as a standard in Great Britain, as currently may be questioned, this term in the review is always placed in parentheses ( ). This clinical condition, as verified by this original research in 1996 and review during the period from 2003 to 2005, can is the cause of several learning disorders, such as dyslexia and dysgraphia, besides the already known consequences such as cerebral palsy and death of the baby . This research (theoretical and practical) was originally carried out with eighty children in 1996/1997 and, in their review (theoretical and practical) between 2003 and 2005, approximately thirty children that born 80% in Brazil, 10% in France and 10% in U.S. In this review of the literature, in 2017, we reviewed the main books cited and included two printed books in addition to online references. These foundations based on the hypothesis of absence of oxygen during birth cause acquired dyslexia, acquired dysgraphia and other learning disorders.
Sergey M. Zimatkin*,Lizaveta I. Bon
The aim of the paper was to estimate histologically the consequences of alcohol consumption by rats during pregnancy on the brain cortex neurons development in their offspring. Female Wistar rats consumed a 15% solution of ethanol as a single source of drinking (4.64±2.19 g/kg/day) throughout pregnancy, control rats received aquivolume amount of water. The offspring were decapitated on the 2-, 5-, 10-, 20-, 45-, and 90th day after birth and samples of frontal brain cortex were prepared for microscopy histology, histochemistry and electron microscopy. Results: Antenatal alcohol exposure in rats increased, and then reduced the brain cortex thickness, the decrease being noted in the relative amount of brain cortex neurons and the increase in the number of their pathological forms in all time periods of the examination. Electron microscopy showed a significant reduction in the number of mitochondria per um2 of cytoplasm and the total length of their cristae, reduction of the rough endoplasmic reticulum canal length and their clearance expansion, decrease in the bind ribosomes and increase in the free ribosomes number, expansion of the Golgi apparatus cisternae, increase in the lysosome number and size in the cytoplasm of neurons. The histochemical examination revealed the inhibition of NADH-, NADPhH, glucose-6-phosphate dehydrogenase and succinate dehydrogenases as well as activation of lactate dehydrogenase and acid phosphatase. Antenatal alcoholization led to the decrease in the expression of synaptophisin (marker of synaptogenesis) and retarded the maturation of neurons in the frontal cortex, which resulted in the increase in the expression of double cortin, and decrease in the expression of neuronal nuclear antigen. Conclusion: Alcohol consumption by rats during pregnancy induces deep and long-term histological, histochemical, immune histochemical and electron microscopy changes in the brain cortex neurons in postnatal ontogenesis in rat offspring, including early swelling and postpone shrinkage and cessation of growth of brain cortex neurons.
Razvodovsky Y. E.*, Troyan E. I., Doroshenko Ye. M., Smirnov V. Yu., Maksimovich N. Ye.
The efficiency of treatment of ischemic brain damage depends upon integrity of sofisticated conceptions of its pathogenesis. One of the prospective approaches in the development of most comprehensive treatment can be the study of the pool of free amino acids (AAs) as a possible target for the correction in such pathology. Available information does not provide a complete view on the changes of their content under ischemia of various severity. The aim of the study was to evaluate changes in the content of free amino acids and their derivatives in the frontal cortex of the cerebral hemispheres of rats at different terms of unilateral ischemia.
Materials and methods: The changes of pool of A As and their derivatives in the frontal cortex of the cerebral hemispheres at different duration of unilateral cerebral ischemia (UCI) (1 hour, 3 hours, 1 day) were studied in 18 rats. The analyses of the levels of AAs and their derivatives were carried out in the supernatant of protein-free tissue homogenates by reversed-phase liquid chromatography using chromatograph Agilent 1100.
Results: Shifts of AAs content after 3 h of UCI observed included the raise of lysine, branched chain AAs (BCAA) – valine and leucine, depletion of the aromatic AAs (AAA) — tyrosine and tryptophan with the doubled ratio of BCAA/AAA. Moreover, we observed the decrease in the content of asparagine and essential/nonessential AAs and glycogenic/ketogenic AAs ratios. These changes were disappeared after 1 day of UCI.
Conclusions: These results show possible mechanisms of development of the energy and neurotransmitter imbalances and their implications in the function of the brain with pathology studied. It is feasible that limitation on BCAA in this pathology will reduce consequences of mediator disturbancies caused by the deficiency of the precursors of biogenic amines – tyrosine and tryptophan.
Biocore Publishing Group
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