The energy needed by cardiac muscle to maintain proper function is supplied by adenosine Ariphosphate primarily (ATP) production through breakdown of fatty acids. Metabolic cardiomyopathies can be caused by disturbances in metabolism, for example diabetes mellitus, hypertrophy and heart failure or alcoholic cardiomyopathy. Deficiency in enzymes of the mitochondrial beta-oxidation show a varying degree of cardiac manifestation. Aberrations of mitochondrial DNA lead to a wide variety of cardiac disorders, without any obvious correlation between genotype and phenotype. A completely different pathogenetic model comprises cardiac manifestation of systemic metabolic diseases caused by deficiencies of various enzymes in a variety of metabolic pathways. Examples of these disorders are glycogen storage diseases (e.g. glycogenosis type II and III), lysosomal storage diseases (e.g. Niemann-Pick disease, Gaucher disease, I-cell disease, various types of mucopolysaccharidoses, GM1 gangliosidosis, galactosialidosis, carbohydrate-deficient glycoprotein syndromes and Sandhoff's disease). There are some systemic diseases which can also affect the heart, for example triosephosphate isomerase deficiency, hereditary haemochromatosis, CD 36 defect or propionic acidaemia.
Human drug targets are a part of our genome of special relevance to human disease. However, the number and nature of drug target genes has not yet been conclusively assessed. We analyzed involvement in biochemical functions, biological processes and pathways, with chromosome, cellular and tissue distribution of the 392 human drug targets collected in DrugBank. Comparison with the whole human genome reveals their scarcely diverse characteristics, largely dominated by rhodopsin-like 7 transmembrane receptors involved in the neuroactive ligand-receptor interaction pathway and located in the plasma membrane. Drug target genes are frequently expressed in multiple tissues, suggesting drug application in distinct disease classes. Intersections with other clinically relevant gene sets, such as the Mendelian disorder-linked genes and various molecular cancer signatures, are discussed.
A biosensor
for the detection of hepatitis B antibodies in clinical
saliva was developed. Compared to conventional analysis of blood serum,
it offers the advantage of noninvasive collection of samples. Detection
of biomarkers in saliva imposes two major challenges associated with
the low analyte concentration and increased surface fouling. The detection
of minute amounts of hepatitis B antibodies was performed by plasmonically
amplified fluorescence sandwich immunoassay. To have access to specific
detection, we prevented the nonspecific adsorption of biomolecules
present in saliva by brushes of poly[(N-(2-hydroxypropyl)
methacrylamide)-co-(carboxybetaine methacrylamide)]
grafted from the gold sensor surface and post modified with hepatitis
B surface antigen. Obtained results were validated against the response
measured with ELISA at a certified laboratory using serum from the
same patients.
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