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Pathological Interactions (pathological + interaction)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Interactions between microvascular and macrovascular disease in diabetes: pathophysiology and therapeutic implications

DIABETES OBESITY & METABOLISM, Issue 6 2007
Andrew J. Krentz
Convention partitions the complications of diabetes into two main subtypes. First are the diabetes-specific microvascular complications of retinopathy, nephropathy and neuropathy; second are the atherothrombotic macrovascular complications that account for the majority of premature deaths. Pathological interactions between microvascular and macrovascular complications, for example, nephropathy and macrovascular disease, are common. Similar mechanisms and shared risk factors drive the development and progression of both small and large vessel disease. This concept has therapeutic implications. Mounting evidence points to the need for multifactorial strategies to prevent vascular complications in subjects with diabetes and/or the metabolic syndrome. We advocate a combined therapeutic approach that addresses small and large vessel disease. Preferential use should be made of drug regimens that (i) maximize vascular protection, (ii) reduce the risk of iatrogenic vascular damage and (iii) minimize the increasing problem of polypharmacy. [source]

Pathological interactions with the timing of birth and uterine activation

AUSTRALIAN AND NEW ZEALAND JOURNAL OF OBSTETRICS AND GYNAECOLOGY, Issue 6 2007
Roger SMITH
Abstract The physiological processes that regulate the onset of parturition and birth are slowly being elucidated, and the points at which pathology can intervene are becoming more apparent. The data support the view that multiple pathways lead to myometrial activation. The clinical corollary is that combinations of tocolytics that operate via different mechanisms may be more effective than single agents. It may also be necessary to divide preterm labour into groups based on underlying mechanisms and to tailor therapy accordingly. [source]

Alcohol and Hepatitis C Virus,Interactions in Immune Dysfunctions and Liver Damage

ALCOHOLISM, Issue 10 2010
Gyongyi Szabo
Hepatitis C virus infection affects 170 million people worldwide, and the majority of individuals exposed to HCV develop chronic hepatitis leading to progressive liver damage, cirrhosis, and hepatocellular cancer. The natural history of HCV infection is influenced by genetic and environmental factors of which chronic alcohol use is an independent risk factor for cirrhosis in HCV-infected individuals. Both the hepatitis C virus and alcohol damage the liver and result in immune alterations contributing to both decreased viral clearance and liver injury. This review will capture the major components of the interactions between alcohol and HCV infection to provide better understanding for the molecular basis of the dangerous combination of alcohol use and HCV infection. Common targets of HCV and alcohol involve innate immune recognition and dendritic cells, the critical cell type in antigen presentation and antiviral immunity. In addition, both alcohol and HCV affect intracellular processes critical for hepatocyte and immune cell functions including mitochondrial and proteasomal activation. Finally, both chronic alcohol use and hepatitis C virus infection increase the risk of hepatocellular cancer. The common molecular mechanisms underlying the pathological interactions between alcohol and HCV include the modulation of cytokine production, lipopolysaccharide (LPS)-TLR4 signaling, and reactive oxygen species (ROS) production. LPS-induced chronic inflammation is not only a major cause of progressive liver injury and fibrosis, but it can also contribute to modification of the tissue environment and stem cells to promote hepatocellular cancer development. Alteration of these processes by alcohol and HCV produces an environment of impaired antiviral immune response, greater hepatocellular injury, and activation of cell proliferation and dedifferentiation. [source]

Role of translational research advancing the understanding of the pathogenesis of light chain-mediated glomerulopathies

PATHOLOGY INTERNATIONAL, Issue 7 2007
Jiamin Teng
Glomerulopathic light chains engage in pathological interactions with mesangial cells resulting in alterations in glomerular homeostasis. The crucial pathological events are centered in the mesangium and, therefore, research dealing with pathogenesis of these disorders is focused on this glomerular compartment. Particular physicochemical characteristics of these light chains are responsible for their ability to alter mesangial milieu leading to glomerular damage. An in vitro model has been used to dissect the processes involved. This model has been instrumental in providing a solid platform from which to observe in a dynamic fashion how mesangial cells handle pathogenic light chains and the sequential steps that are involved in the progressive glomerular damage. Key steps amenable to possible modulation have been defined and should provide a solid platform to design and test therapeutic interventions. In the past significant difficulties have been encountered in the development of animal models of light chain-induced glomerular damage. However, in the last few years a new generation of animal models has emerged to address whether what has been documented in vitro retains significance in vivo. Preliminary observations appear to substantiate this. [source]