Age-realted dementia in Kazahstan: adaptation of the 10/66 dementia research group population -based study protocol

Background. The prevalence of dementia is increasing worldwide as the population ages and affects 10 % of the population over 65 years old and 40 % of people over the age of 80.[1] In Kazakhstan, as well as in other countries around the world, the population of aged people has been increasing over the past decades. According to available statistics, by the end of 2013, the percentage of people aged 65 and older in Kazakhstan was 6.7% [2]. Given the fact that Kazakhstan's current population is about 17,221 million people [2], and based on data from the global statistics, it can be assumed that at least 115,000 elderly people could be suffering from age-related dementia. Nevertheless, such pathology is currently may not being diagnosed in Kazakhstan; consequently giving no accurate statistical data on the number of people suffering from this age-related pathology. Thus, the aim of this study is to estimate true prevalence of dementia and assess the risk factors associated with the disease

Age-realted dementia in Kazahstan: adaptation of the 10/66 dementia research group population -based study protocol

Background. The prevalence of dementia is increasing worldwide as the population ages and affects 10 % of the population over 65 years old and 40 % of people over the age of 80.[1] In Kazakhstan, as well as in other countries around the world, the population of aged people has been increasing over the past decades. According to available statistics, by the end of 2013, the percentage of people aged 65 and older in Kazakhstan was 6.7% [2]. Given the fact that Kazakhstan's current population is about 17,221 million people [2], and based on data from the global statistics, it can be assumed that at least 115,000 elderly people could be suffering from age-related dementia. Nevertheless, such pathology is currently may not being diagnosed in Kazakhstan; consequently giving no accurate statistical data on the number of people suffering from this age-related pathology. Thus, the aim of this study is to estimate true prevalence of dementia and assess the risk factors associated with the disease

Small molecule targeting of the p38/Mk2 stress signaling pathways to improve cancer treatment

Purpose: Although a long-term goal of cancer therapy always has been the development of agents that selectively destroy cancer cells, more recent trends have been to seek secondary agents that sensitize cancer cells to existing treatment regimens. In this regard, the present study explored the possibility of using small molecule inhibitors of p38MAPK/MK2 stress signaling pathways as potential agents to enhance the sensitivity of cancer cells with abrogated G1 checkpoint to the DNA damaging agent etoposide by specifically targeting the DNA damage-induced G2 cell cycle checkpoint. Methods: We have applied CCK8 and FACS-based viability assays and cell cycle analysis to investigate the effect of small molecules SB203580 and MK2.III on the sensitivity of small cell lung cancer cells (SCLC) that lack the G1 checkpoint to the DNA damaging agent Etoposide when used in combination. We have also assessed the effectiveness of combination chemotherapy on tumor xenograft suppression with etoposide and MK2.III in immunosuppressed mice. In addition, additional CCK8 cell viability analysis of the MDA-MB-231 breast cancer cell line, and SW620, and SW480 colorectal cancer cell lines was performed. Results: Results suggest that etoposide produces a profound effect on the cell cycle profile of cells in a manner that is consistent with the degree of cell viability that is seen using the viable cell assay. Results of the co-treatment experiments revealed that the p38/MK2 kinase inhibitors SB203580 and MK2.III both enhanced the DNA-damaging effects of etoposide on NCI-H69 cell viability in vitro. Results revealed that in vivo MK2.III was able to act as a chemosensitizer when used in combination with etoposide making NCI-H69 lung cancer cells sensitive to chemotherapeutic drug by 45% compared to single usage of the drug. We also report that MK2.III sensitizes metastatic cell lines SW-620 and MDA-MB-231 to etoposide but does not increase the sensitivity of non-metastasizing SW-480 colorectal cells to DNA damaging agent in vitro. Conclusion: Findings reported in this study provide evidence that specific inhibitors of MK2 may indeed improve overall cancer therapy; however, their effectiveness depends on cell types

Combining vitamin C and carotenoid biomarkers better predicts fruit and vegetable intake than individual biomarkers in dietary intervention studies.

The aim of this study was to determine whether combining potential biomarkers of fruit and vegetables is better at predicting FV intake within FV intervention studies than single biomarkers

Establishment of small cell lung cancer cell lines and validation of their growth characteristics

Rapidly metastasizing lung cancer is the top killer in the United States and many other countries. In 2014, there were nearly 224 210 new cases of lung cancer and 159 260 predicted mortality from the disease in the US and approximately 44 488 new registered cases of lung cancer in 2012 with 80% mortality and 5 % survival rate within 10 years of diagnosis in the UK. Lung cancer is the most prevalent type of cancer in Kazakhstan accounting for nearly 22.1 % of all cancer cases. Small cell lung cancers (SCLCs) derived from the hormonal cells of the lung and classified as one of the most dedifferentiated cancers representing 10 - 15% of all lung cancers however showing extremely aggressive and rapid dissemination into various parts of the body. In this work we established SCLC cell line and characterised their growth for upcoming research purposes

Establishment of small cell lung cancer cell lines and validation of their growth characteristics

Rapidly metastasizing lung cancer is the top killer in the United States and many other countries. In 2014, there were nearly 224 210 new cases of lung cancer and 159 260 predicted mortality from the disease in the US and approximately 44 488 new registered cases of lung cancer in 2012 with 80% mortality and 5 % survival rate within 10 years of diagnosis in the UK. Lung cancer is the most prevalent type of cancer in Kazakhstan accounting for nearly 22.1 % of all cancer cases. Small cell lung cancers (SCLCs) derived from the hormonal cells of the lung and classified as one of the most dedifferentiated cancers representing 10 - 15% of all lung cancers however showing extremely aggressive and rapid dissemination into various parts of the body. In this work we established SCLC cell line and characterised their growth for upcoming research purposes

Role of astrocyte aging in the pathogenesis of alzheimer`s disease

Alzheimer's disease (AD) is the most abundant severe and irreversible neurodegenerative disease in the world that affects people over 65 years old. The major hallmarks of AD pathology are the senile p-amyloid plaques, hyperphosphorylated neurofibrillary tangles, accompanied by severe neuroinflammation, synaptic disruption, neuronal degeneration and apoptosis, eventually triggering cerebral atrophy, memory loss and cognitive decline. The deposition and increase of p-amyloid levels in the brain induce the cascade of signals triggering production of neurotoxic molecules such as reactive oxygen species, nitric oxide, and proinflammatory cytokines and chemokines that cause neuroinflammation and neurodegeneration eventually resulting into dementia. Aging is the key risk factor for many inflammatory diseases including AD. However, the correlation of aging and AD is poorly investigated. Especially, the cytotoxic effects of p-amyloid in aging glial cells have been poorly explored. Human astrocytes are the most abundant CNS cells that undergo senescence with age and in response to stress. Therefore, it is hypothesized that sensitivity to p-amyloid may significantly change during in vitro senescence of astrocytes. The aim of this study is to investigate the mechanisms of cytotoxic actions of p-amyloid peptide in senescent astrocytes

Role of astrocyte aging in the pathogenesis of alzheimer`s disease

Alzheimer's disease (AD) is the most abundant severe and irreversible neurodegenerative disease in the world that affects people over 65 years old. The major hallmarks of AD pathology are the senile p-amyloid plaques, hyperphosphorylated neurofibrillary tangles, accompanied by severe neuroinflammation, synaptic disruption, neuronal degeneration and apoptosis, eventually triggering cerebral atrophy, memory loss and cognitive decline. The deposition and increase of p-amyloid levels in the brain induce the cascade of signals triggering production of neurotoxic molecules such as reactive oxygen species, nitric oxide, and proinflammatory cytokines and chemokines that cause neuroinflammation and neurodegeneration eventually resulting into dementia. Aging is the key risk factor for many inflammatory diseases including AD. However, the correlation of aging and AD is poorly investigated. Especially, the cytotoxic effects of p-amyloid in aging glial cells have been poorly explored. Human astrocytes are the most abundant CNS cells that undergo senescence with age and in response to stress. Therefore, it is hypothesized that sensitivity to p-amyloid may significantly change during in vitro senescence of astrocytes. The aim of this study is to investigate the mechanisms of cytotoxic actions of p-amyloid peptide in senescent astrocytes