Background: Our previous study analyzed the age trajectory of mortality (ATM) in 14 European countries, while this study aimed at investigating ATM in other continents and in countries with a higher level of mortality. Data from 11 Non-European countries were used. Methods: The number of deaths was extracted from the WHO mortality database. The Halley method was used to calculate the mortality rates in all possible calendar years and all countries combined. This method enables us to combine more countries and more calendar years in one hypothetical population. Results: The age trajectory of total mortality (ATTM) and also ATM due to specific groups of diseases were very similar in the 11 non-European countries and in the 14 European countries. The level of mortality did not affect the main results found in European countries. The inverse proportion was valid for ATTM in non-European countries with two exceptions. Slower or no mortality decrease with age was detected in the first year of life, while the inverse proportion model was valid for the age range (1, 10) years in most of the main chapters of ICD10. Conclusions: The decrease in child mortality with age may be explained as the result of the depletion of individuals with congenital impairment. The majority of deaths up to the age of 10 years were related to congenital impairments, and the decrease in child mortality rate with age was a demonstration of population heterogeneity. The congenital impairments were latent and may cause death even if no congenital impairment was detected.

• Klíčová slova
• WHO database, age, childhood, congenital anomalies, mortality rate,
• Publikační typ
• časopisecké články MeSH

Background: Mortality rate rapidly decreases with age after birth, and, simultaneously, the spectrum of death causes show remarkable changes with age. This study analyzed age-associated decreases in mortality rate from diseases of all main chapters of the 10th revision of the International Classification of Diseases. Methods: The number of deaths was extracted from the mortality database of the World Health Organization. As zero cases could be ascertained for a specific age category, the Halley method was used to calculate the mortality rates in all possible calendar years and in all countries combined. Results: All causes mortality from the 1st day of life to the age of 10 years can be represented by an inverse proportion model with a single parameter. High coefficients of determination were observed for total mortality in all populations (arithmetic mean = 0.9942 and standard deviation = 0.0039). Slower or no mortality decrease with age was detected in the 1st year of life, while the inverse proportion method was valid for the age range [1, 10) years in most of all main chapters with three exceptions. The decrease was faster for the chapter "Certain conditions originating in the perinatal period" (XVI).The inverse proportion was valid already from the 1st day for the chapter "Congenital malformations, deformations and chromosomal abnormalities" (XVII).The shape of the mortality decrease was very different for the chapter "Neoplasms" (II) and the rates of mortality from neoplasms were age-independent in the age range [1, 10) years in all populations. Conclusion: The theory of congenital individual risks of death is presented and can explain the results. If it is valid, latent congenital impairments may be present among all cases of death that are not related to congenital impairments. All results are based on published data, and the data are presented as a supplement.

• Klíčová slova
• WHO database, age, childhood, congenital anomalies, mortality rate,
• Publikační typ
• časopisecké články MeSH

Background: In humans, the mortality rate dramatically decreases with age after birth, and the causes of death change significantly during childhood. In the present study, we attempted to explain age-associated decreases in mortality for congenital anomalies of the central nervous system (CACNS), as well as decreases in total mortality with age. We further investigated the age trajectory of mortality in the biologically related category "diseases of the nervous system" (DNS). Methods: The numbers of deaths were extracted from the mortality database of the World Health Organization (WHO) for the following nine countries: Denmark, Finland, Norway, Sweden, Austria, the Czech Republic, Hungary, Poland, and Slovakia. Because zero cases could be ascertained over the age of 30 years in a specific age category, the Halley method was used to calculate the mortality rates in all possible calendar years and in all countries combined. Results: Total mortality from the first day of life up to the age of 10 years and mortality due to CACNS within the age interval of [0, 90) years can be represented by an inverse proportion with a single parameter. High coefficients of determination were observed for both total mortality (R2 = 0.996) and CACNS mortality (R2 = 0.990). Our findings indicated that mortality rates for DNS slowly decrease with age during the first 2 years of life, following which they decrease in accordance with an inverse proportion up to the age of 10 years. The theory of congenital individual risk (TCIR) may explain these observations based on the extinction of individuals with more severe impairments, as well as the bent curve of DNS, which exhibited an adjusted coefficient of determination of R¯2 = 0.966. Conclusion: The coincidence between the age trajectories of all-cause and CACNS-related mortality may indicate that the overall decrease in mortality after birth is due to the extinction of individuals with more severe impairments. More deaths unrelated to congenital anomalies may be caused by the manifestation of latent congenital impairments during childhood.

• Klíčová slova
• WHO database, age, childhood, congenital anomalies of the central nervous system, mortality rate,
• Publikační typ
• časopisecké články MeSH

Telomerase is an enzyme that adds repeats of DNA sequences to the ends of chromosomes, thereby preventing their shortening. Telomerase activity is associated with proliferative status of cells, organismal development, and aging. We report an analysis of telomerase activity and telomere length in the honeybee, Apis mellifera. Telomerase activity was found to be regulated in a development and caste-specific manner. During the development of somatic tissues of larval drones and workers, telomerase activity declined to 10 % of its level in embryos and remained low during pupal and adult stages but was upregulated in testes of late pupae, where it reached 70 % of the embryo level. Upregulation of telomerase activity was observed in the ovaries of late pupal queens, reaching 160 % of the level in embryos. Compared to workers and drones, queens displayed higher levels of telomerase activity. In the third larval instar of queens, telomerase activity reached the embryo level, and an enormous increase was observed in adult brains of queens, showing a 70-fold increase compared to a brain of an adult worker. Southern hybridization of terminal TTAGG fragments revealed a high variability of telomeric length between different individuals, although the same pattern of hybridization signals was observed in different tissues of each individual.

• Klíčová slova
• Apis mellifera, Insects, Longevity, Telomerase, Telomere,
• MeSH
• chromozomy hmyzu genetika   metabolismus   MeSH
• hmyzí proteiny genetika   metabolismus   MeSH
• homeostáza telomer fyziologie   MeSH
• telomerasa genetika   metabolismus   MeSH
• telomery genetika   metabolismus   MeSH
• včely genetika   metabolismus   MeSH
• zvířata MeSH
• Check Tag
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• hmyzí proteiny MeSH
• telomerasa MeSH

Alzheimer's disease (AD) is the most common form of dementia. The risk of AD increases with age. Although two of the main pathological features of AD, amyloid plaques and neurofibrillary tangles, were already recognized by Alois Alzheimer at the beginning of the 20th century, the pathogenesis of the disease remains unsettled. Therapeutic approaches targeting plaques or tangles have not yet resulted in satisfactory improvements in AD treatment. This may, in part, be due to early-onset and late-onset AD pathogenesis being underpinned by different mechanisms. Most animal models of AD are generated from gene mutations involved in early onset familial AD, accounting for only 1% of all cases, which may consequently complicate our understanding of AD mechanisms. In this article, the authors discuss the pathogenesis of AD according to the two main neuropathologies, including senescence-related mechanisms and possible treatments using stem cells, namely mesenchymal and neural stem cells.

• Klíčová slova
• Alzheimer’s disease, Tau, amyloid-β, mesenchymal stem cells, neural stem cells,
• MeSH
• Alzheimerova nemoc etiologie   metabolismus   patologie   terapie   MeSH
• amyloidní beta-protein imunologie   metabolismus   MeSH
• amyloidní plaky metabolismus   patologie   MeSH
• buněčná a tkáňová terapie * metody   MeSH
• energetický metabolismus MeSH
• imunoterapie metody   MeSH
• kmenové buňky cytologie   metabolismus   MeSH
• lidé MeSH
• modely nemocí na zvířatech MeSH
• mutace MeSH
• neuroglie metabolismus   MeSH
• proteiny tau imunologie   metabolismus   MeSH
• stárnutí genetika   imunologie   metabolismus   MeSH
• transplantace kmenových buněk metody   MeSH
• věk při počátku nemoci MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• amyloidní beta-protein MeSH
• proteiny tau MeSH