Wyniki wyszukiwania

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The influence of moderate-intensity physical effort on peripheral blood in adults with Down syndrome - a pilot study

100%

Aleksander-Szymanowicz P., Marchewka A., Dabrowski Z., Teleglow A., Bac A., Glodzik J.

Journal of Physiology and Pharmacology

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2014

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tom 65

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nr 5

2

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Mapping of India’s contribution on “Down syndrome” during 40 years from 1973-2012

100%

Siwach A. K.

International Letters of Natural Sciences

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2015

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tom 07

Down syndrome, a genetic disease, is commonly diagnosed congenital malformation/mental retardation syndrome occurring in people of all races and economic levels. The present study is aimed to examine the contribution of Indian scientists on Down syndrome during the 40 years span from 1973-2012. The study analyses the Indian share in the research output, contribution and citation impact of top Indian institutions, most prolific Indian authors, top journals for publication, top collaborating countries, number of citations received and the highly cited papers in the Indian research on Down syndrome.

3

Down syndrome - genetic and nutritional aspects of accompanying disorders

84%

Mazurek D., Wyka J.

Roczniki Państwowego Zakładu Higieny

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2015

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tom 66

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nr 3

Down syndrome (DS) is one of the more commonly occurring genetic disorders, where mental retardation is combined with nutritional diseases. It is caused by having a third copy of chromosome 21, and there exist 3 forms; Simple Trisomy 21, Translocation Trisomy and Mosaic Trisomy. Symptoms include intellectual disability/mental retardation, early onset of Alzheimer’s disease and the appearance of various phenotypic features such as narrow slanted eyes, flat nose and short stature. In addition, there are other health problems throughout the body, consisting in part of cardiac defects and thyroid function abnormalities along with nutritional disorders (ie. overweight, obesity, hypercholesterolemia and deficiencies of vitamins and minerals). Those suffering DS have widespread body frame abnormalities and impaired brain development and function; the latter leading to impaired intellectual development. Many studies indicate excessive or deficient nutrient uptakes associated with making inappropriate foodstuff choices, food intolerance, (eg. celiac disease) or malabsorption. DS persons with overweight or obesity are linked with a slow metabolic rate, abnormal blood leptin concentrations and exhibit low levels of physical activity. Vitamin B group deficiencies and abnormal blood homocysteine levels decrease the rate of intellectual development in DS cases. Zinc deficiencies result in short stature, thyroid function disorders and an increased appetite caused by excessive supplementation. Scientific advances in the research and diagnosis of DS, as well as preventing any associated conditions, have significantly increased life expectancies of those with this genetic disorder. Early dietary interventions by parents or guardians of DS children afford an opportunity for decreasing the risk or delaying some of the DS associated conditions from appearing, thus beneficially impacting on their quality of life.

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The induction of apoptosis by daunorubicin and idarubicin in human trisomic and diabetic fibroblasts

84%

Dragojew S., Marczak A., Maszewski J., Ilnicki K., Jozwiak Z.

Cellular and Molecular Biology Letters

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2008

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tom 13

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nr 2

182-194

In this study, we investigated apoptosis induced in human trisomic and diabetic fibroblasts by daunorubicin (DNR) and its derivative, idarubicin (IDA). The cells were incubated with DNR or IDA for 2 h and then cultured in a drug-free medium for a further 2–48 h. The apoptosis in the cultured cell lines was assessed by biochemical analysis. We found that both drugs induced a timedependent loss of mitochondrial membrane potential, and a significant increase in intracellular calcium and caspase-3 activity. Mitochondrial polarization and changes in the level of intracellular calcium were observed during the first 2–6 h after drug treatment. Caspase-3 activation occurred in the late stages of the apoptotic pathway. Our findings also demonstrated that idarubicin was more cytotoxic and more effective than daunorubicin in inducing apoptosis in trisomic and diabetic fibroblasts.

5

Alzheimer's amyloid-beta [Abeta] is an essential synaptic protein, not neurotoxic junk

84%

Koudinov A. R., Berezov T. T.

Acta Neurobiologiae Experimentalis

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2004

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tom 64

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nr 1

6

Anti-inflammatory plasma cytokines in children and adolescents with Down syndrome

67%

Smigielska-Kuzia J., Bockowski L., Sobaniec W., Sendrowski K., Zelazowska-Rutkowska B., Cholewa M.

Folia Histochemica et Cytobiologica

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2010

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tom 48

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nr 4

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Aneuploidy, chromosomal missegregation, and cell cycle reentry in Alzheimer's disease

67%

Zekanowski C., Wojda U.

Acta Neurobiologiae Experimentalis

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2009

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tom 69

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nr 2

232-253

Alzheimer's disease (AD) is a neurodegenerative disorder with a complex etiology and pathogenesis. Chromosome missegregation was proposed two decades ago to be responsible for neurodegeneration in AD patients. It was speculated that the aneuploidy is a result of aberrant cell cycle of neuronal progenitors during adult neurogenesis and/or of mature neurons. There is mounting evidence of increased rate of general aneuploidy and cell cycle reentry in the AD patients' brains, with area-specific pattern. In this review, we discuss the involvement of chromosome instability, genome damage and cell cycle impairment in AD pathology.

Ograniczanie wyników

The influence of moderate-intensity physical effort on peripheral blood in adults with Down syndrome - a pilot study

Mapping of India’s contribution on “Down syndrome” during 40 years from 1973-2012

Down syndrome - genetic and nutritional aspects of accompanying disorders

The induction of apoptosis by daunorubicin and idarubicin in human trisomic and diabetic fibroblasts

Alzheimer's amyloid-beta [Abeta] is an essential synaptic protein, not neurotoxic junk

Anti-inflammatory plasma cytokines in children and adolescents with Down syndrome

Aneuploidy, chromosomal missegregation, and cell cycle reentry in Alzheimer's disease