Examining Universal Primary Healthcare Through Community-Based Initiatives

This paper examines enacting community-based primary healthcare programs and initiatives. It looks at the weaknesses of past attempts, the successes of current attempts, and gives insight into ways everyday citizens can change the way the world does healthcare. There are social, economic, and political barriers as to why these programs are not enacted. Since 1978, Member states of the United Nations strive towards healthcare for all. The original 1978 Declaration of Alma-Ata sets the bar at achieving this goal by the year 2000. Now in the 21st century, the world still battles inadequate healthcare. Nations continue to strive towards the goal of health for all, and many healthcare professionals advocate for enacting community-based initiatives. This paper seeks to bring light to the issues of modern healthcare, and hopes to encourage everyone to support community-based programs so that in the near future the world can have true health for all

The Extent of Indigenous-Norse Contact and Trade Prior to Columbus

Norse exploration during the medieval period was widespread and diverse in location. Of the many places visited by the Norse, North America has continued to be surrounded by mystery. The full extent of Norse exploration in North America is a growing field and the extent of their contact and trade with Indigenous Americans is becoming increasingly known. A thorough compilation of the evidence allows for significant, new conclusions to be made about Norse presence in the Americas

Peripheral reductive capacity is associated with cognitive performance and survival in Alzheimer's disease

BACKGROUND: Oxidative stress is believed to be an early event and a key factor in Alzheimer's disease (AD) pathogenesis and progression. In spite of an intensive search for surrogate markers to monitor changes related to oxidative stress in the brain, there is as yet no consensus about which markers to use in clinical studies. The measurement of peripheral anti-oxidants is an alternative way of evaluating the involvement of oxidative stress in the course of the disease. Given the complexity of peripheral anti-oxidant defence, variations in the levels of individual anti-oxidant species may not fully reflect the overall capacity to fight oxidant conditions. We therefore chose to evaluate the total reductive capacity (herein defined as anti-oxidant capacity, AOC) in serum from control subjects and AD patients in order to study the association between peripheral anti-oxidant defence, cognitive impairment and patient survival. METHODS: We measured the levels of AOC in serum samples from 26 cognitively normal controls and 25 AD patients (12 post-mortem confirmed) who completed the Cambridge Cognitive Assessment. Cognitive decline was assessed in a subgroup of 19 patients who underwent a second cognitive assessment 2 years after the initial visit. RESULTS: Serum AOC levels were lower in AD patients than in controls and were correlated with their cognitive test scores, although AOC levels were unrelated to cognitive decline assessed two years later. On the other hand, AOC levels were predictive of the length of patients' survival, with higher levels giving longer survival. CONCLUSION: This study indicates that peripheral anti-oxidant defences are depleted in AD patients. The results suggest that serum AOC is a good index of the general health status and prognosis of patients but does not necessarily reflect the extent to which vulnerable neuronal populations are protected from oxidant processes. Further studies are required to establish whether peripheral AOC measurements may be useful in identifying asymptomatic individuals or those with early symptoms at high risk of developing significant cognitive impairment or dementia

Replication of the association of HLA-B7 with Alzheimer's disease: a role for homozygosity?

BACKGROUND: There are reasons to expect an association with Alzheimer's disease (AD) within the HLA region. The HLA-B & C genes have, however, been relatively understudied. A geographically specific association with HLA-B7 & HLA-Cw*0702 had been suggested by our previous, small study. METHODS: We studied the HLA-B & C alleles in 196 cases of 'definite' or 'probable' AD and 199 elderly controls of the OPTIMA cohort, the largest full study of these alleles in AD to date. RESULTS: We replicated the association of HLA-B7 with AD (overall, adjusted odds ratio = 2.3, 95% confidence interval = 1.4–3.7, p = 0.001), but not the previously suggested interaction with the ε4 allele of apolipoprotein E. Results for HLA-Cw*0702, which is in tight linkage disequilibrium with HLA-B7, were consistent with those for the latter. Homozygotes of both alleles appeared to be at particularly high risk of AD. CONCLUSION: HLA-B7 and HLA-Cw*0702 are associated with AD in the Oxford population. Because of the contradictions between cohorts in our previous study, we suggest that these results may be geographically specific. This might be because of differences between populations in the structure of linkage disequilibrium or in interactions with environmental, genetic or epigenetic factors. A much larger study will be needed to clarify the role of homozygosity of HLA alleles in AD risk

Interaction of nutrition and genetics via DNMT3L-mediated DNA methylation determines cognitive decline

Low homocysteine levels and B vitamin treatment are reported to protect against declining cognitive health. Both B vitamins and homocysteine are involved in the production of S-adenosylmethionine, a universal methyl donor essential for the process of DNA methylation. We investigated the effect of a damaging coding variant within the DNA methyltransferase gene, DNMT3L (R278G, A/G) by examining B vitamin intake, homocysteine levels, cognitive performance, and brain atrophy in individuals in the VITACOG study of Mild Cognitive Impairment and the TwinsUK cohort. In the VITACOG study, individuals who received a two- year treatment of B vitamins and carried the G allele, showed better ‘visuospatial associative memory’ and slower rates of brain atrophy. In the TwinsUK study, improved ‘visuospatial associative memory’ was evident in individuals who reported regular vitamin intake and were A/A homozygotes. In silico modelling indicated that R278G disrupts protein interaction between DNMT3L and DNMT3A, affecting the DNMT3A-3L-H3 complex required for DNA methylation. These findings show that vitamin intake and genetic variation within DNMT3L interact to influence cognitive decline

Practical detection of a definitive biomarker panel for Alzheimer's disease: comparisons between matched plasma and cerebrospinal fluid

Previous mass spectrometry analysis of cerebrospinal fluid (CSF) has allowed the identification of a panel of molecular markers that are associated with Alzheimer’s disease (AD). The panel comprises Amyloid beta, Apolipoprotein E, Fibrinogen alpha chain precursor, Keratin type I cytoskeletal 9, Serum albumin precursor, SPARC-like 1 protein and Tetranectin. Here we report the development and implementation of immunoassays to measure the abundance and diagnostic capacity of these putative biomarkers in matched lumbar CSF and blood plasma samples taken in life from individuals confirmed at post-mortem as suffering from AD (n=10) and from screened ‘cognitively healthy’ subjects (n=18). The inflammatory components of Alzheimer’s disease were also investigated. Employment of supervised learning techniques permitted examination of the interrelated expression patterns of the putative biomarkers and identified inflammatory components, resulting in biomarker panels with a diagnostic accuracy of 87.5% and 86.7% for the plasma and CSF datasets respectively. This is extremely important as it offers an ideal high-throughput and relatively inexpensive population screening approach. It appears possible to determine the presence or absence of AD based on our biomarker panel and it seems likely that a cheap and rapid blood test for AD is feasible

Practical detection of a definitive biomarker panel for Alzheimer's disease: comparisons between matched plasma and cerebrospinal fluid

Previous mass spectrometry analysis of cerebrospinal fluid (CSF) has allowed the identification of a panel of molecular markers that are associated with Alzheimer’s disease (AD). The panel comprises Amyloid beta, Apolipoprotein E, Fibrinogen alpha chain precursor, Keratin type I cytoskeletal 9, Serum albumin precursor, SPARC-like 1 protein and Tetranectin. Here we report the development and implementation of immunoassays to measure the abundance and diagnostic capacity of these putative biomarkers in matched lumbar CSF and blood plasma samples taken in life from individuals confirmed at post-mortem as suffering from AD (n=10) and from screened ‘cognitively healthy’ subjects (n=18). The inflammatory components of Alzheimer’s disease were also investigated. Employment of supervised learning techniques permitted examination of the interrelated expression patterns of the putative biomarkers and identified inflammatory components, resulting in biomarker panels with a diagnostic accuracy of 87.5% and 86.7% for the plasma and CSF datasets respectively. This is extremely important as it offers an ideal high-throughput and relatively inexpensive population screening approach. It appears possible to determine the presence or absence of AD based on our biomarker panel and it seems likely that a cheap and rapid blood test for AD is feasible

Visual function, traumatic brain injury, and posttraumatic stress disorder

Traumatic brain injury (TBI) and posttraumatic stress disorder (PTSD) are signature injuries of the Iraq and Afghanistan conflicts. The conditions can be comorbid and have overlapping signs and symptoms, making it difficult to diagnose and treat each. TBI is associated with numerous changes in vision function, but vision problems secondary to PTSD have not been documented. To address this shortcoming, we reviewed the medical records of 100 patients with a history of TBI, noting PTSD diagnoses, visual symptoms, vision function abnormalities, and medications with visual side effects. Forty-one patients had PTSD and 59 did not. High rates of binocular vision and oculomotor function deficits were measured in patients with a history of TBI, but no significant differences between patients with or without PTSD were evident. However, compared to patients without PTSD, patients with PTSD had more self-reported visual symptoms in all four assessments and the complaint rates were significantly higher for light sensitivity and reading problems. Together, these findings may be beneficial in understanding vision problems in patients with TBI and PTSD as comorbid conditions compared with those with TBI alone