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Diseases, Volume 1, Issue 1 (December 2013) – 4 articles , Pages 1-72

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299 KiB  
Review
Effect of Cardio-Metabolic Risk Factors Clustering with or without Arterial Hypertension on Arterial Stiffness: A Narrative Review
by Vasilios G. Athyros, Andromachi Reklou, Antonis Lazarides, Eudoxia Mitsiou and Asterios Karagiannis
Diseases 2013, 1(1), 51-72; https://doi.org/10.3390/diseases1010051 - 20 Nov 2013
Viewed by 6225
Abstract
The clustering of cardio-metabolic risk factors, either when called metabolic syndrome (MetS) or not, substantially increases the risk of cardiovascular disease (CVD) and causes mortality. One of the possible mechanisms for this clustering's adverse effect is an increase in arterial stiffness (AS), and [...] Read more.
The clustering of cardio-metabolic risk factors, either when called metabolic syndrome (MetS) or not, substantially increases the risk of cardiovascular disease (CVD) and causes mortality. One of the possible mechanisms for this clustering's adverse effect is an increase in arterial stiffness (AS), and in high central aortic blood pressure (CABP), which are significant and independent CVD risk factors. Arterial hypertension was connected to AS long ago; however, other MetS components (obesity, dyslipidaemia, dysglycaemia) or MetS associated abnormalities not included in MetS diagnostic criteria (renal dysfunction, hyperuricaemia, hypercoaglutability, menopause, non alcoholic fatty liver disease, and obstructive sleep apnea) have been implicated too. We discuss the evidence connecting these cardio-metabolic risk factors, which negatively affect AS and finally increase CVD risk. Furthermore, we discuss the impact of possible lifestyle and pharmacological interventions on all these cardio-metabolic risk factors, in an effort to reduce CVD risk and identify features that should be taken into consideration when treating MetS patients with or without arterial hypertension. Full article
(This article belongs to the Special Issue Feature Papers)
205 KiB  
Review
The Nervous System Cytoskeleton under Oxidative Stress
by John Gardiner, Robyn Overall and Jan Marc
Diseases 2013, 1(1), 36-50; https://doi.org/10.3390/diseases1010036 - 21 Oct 2013
Cited by 15 | Viewed by 6919
Abstract
Oxidative stress is a key mechanism causing protein aggregation, cell death and neurodegeneration in the nervous system. The neuronal cytoskeleton, that is, microtubules, actin filaments and neurofilaments, plays a key role in defending the nervous system against oxidative stress-induced damage and is also [...] Read more.
Oxidative stress is a key mechanism causing protein aggregation, cell death and neurodegeneration in the nervous system. The neuronal cytoskeleton, that is, microtubules, actin filaments and neurofilaments, plays a key role in defending the nervous system against oxidative stress-induced damage and is also a target for this damage itself. Microtubules appear particularly susceptible to damage, with oxidative stress downregulating key microtubule-associated proteins [MAPs] and affecting tubulin through aberrant post-translational modifications. Actin filaments utilise oxidative stress for their reorganisation and thus may be less susceptible to deleterious effects. However, because cytoskeletal components are interconnected through crosslinking proteins, damage to one component affects the entire cytoskeletal network. Neurofilaments are phosphorylated under oxidative stress, leading to the formation of protein aggregates reminiscent of those seen in neurodegenerative diseases. Drugs that target the cytoskeleton may thus be of great use in treating various neurodegenerative diseases caused by oxidative stress. Full article
(This article belongs to the Special Issue Feature Papers)
108 KiB  
Review
The Complex Nature of Adherence in the Management of HIV/AIDS as a Chronic Medical Condition
by Adegoke O. Adefolalu and Zerish Z. Nkosi
Diseases 2013, 1(1), 18-35; https://doi.org/10.3390/diseases1010018 - 13 Sep 2013
Cited by 13 | Viewed by 8418
Abstract
The introduction of antiretroviral therapy (ART) in the management of HIV infection has resulted in a significant reduction in the morbidity and mortality associated with the disease. The fact that a nearly perfect adherence is required in ART has remained a major challenge [...] Read more.
The introduction of antiretroviral therapy (ART) in the management of HIV infection has resulted in a significant reduction in the morbidity and mortality associated with the disease. The fact that a nearly perfect adherence is required in ART has remained a major challenge to people infected with HIV. This review underscores the impact of adherence to antiretroviral therapy and highlights recent advances in adherence monitoring and enhancement among people infected with HIV who are on lifelong antiretroviral therapy. Full article
1004 KiB  
Article
Protein Kinase C Epsilon Contributes to NADPH Oxidase Activation in a Pre-Eclampsia Lymphoblast Cell Model
by Toryn M. Poolman, Paulene A. Quinn and Leong Ng
Diseases 2013, 1(1), 1-17; https://doi.org/10.3390/diseases1010001 - 28 Aug 2013
Cited by 3 | Viewed by 6024
Abstract
Pre-eclampsia is a pregnancy-specific disorder characterised by hypertension and proteinuria, which in severe cases results in multi-system disturbances. The maternal syndrome is associated with a pro-inflammatory state, consisting of leukocyte activation, which is thought to contribute to the widespread endothelial dysfunction. We previously [...] Read more.
Pre-eclampsia is a pregnancy-specific disorder characterised by hypertension and proteinuria, which in severe cases results in multi-system disturbances. The maternal syndrome is associated with a pro-inflammatory state, consisting of leukocyte activation, which is thought to contribute to the widespread endothelial dysfunction. We previously showed increased activation of NADPH oxidase in pre-eclampsia, in both neutrophils and B-lymphoblast cell lines (B-LCLs). In this study, the mechanism by which NADPH oxidase activity is increased in pre-eclampsia was further investigated. NADPH oxidase activity was found to be increased in phorbol-12-myristate-13-acetate (PMA) stimulated B-LCLs isolated from women with pre-eclampsia. This correlated with an increase in protein kinase C (PKC) substrate phosphorylation, p47-phox phosphorylation (a regulatory component of NADPH oxidase) and p47-phox directed-kinase activity. Using ion exchange and hydroxyapatite chromatography we identified a major peak of PMA regulated p47-phox kinase activity. Chromatography fractions were probed for PKC isoforms. We found the major peak of p47-phox kinase activity could not be separated from the elution profile of PKC epsilon. Using a peptide inhibitor of PKC epsilon, PMA-induced reactive oxygen species (ROS) production could be reduced to that of a normal B-LCL. These data suggest a pro-inflammatory role for PKC epsilon in the pathogenesis of pre-eclampsia. Full article
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