Written for tradesmen, "Liber Abaci" laid out Hindu-Arabic arithmetic useful for tracking profits, losses, remaining loan balances and so on, Devlin said. In one place in the book, Leonardo of Pisa introduces the sequence with a problem involving rabbits. The problem goes as follows: Start with a male and a female rabbit. After a month, they mature and produce a litter with another male and female rabbit. A month later, those rabbits reproduce and out comes — you guessed it — another male and female, who also can mate after a month.
Ventricular fibrillation - Wikipedia
Ignore the wildly improbable biology here. After a year, how many rabbits would you have? But after a few scant paragraphs on breeding rabbits, Leonardo of Pisa never mentioned the sequence again. In fact, it was mostly forgotten until the 19th century, when mathematicians worked out more about the sequence's mathematical properties. But what exactly is the significance of the Fibonacci sequence? Other than being a neat teaching tool, it shows up in a few places in nature.
Atrial Flutter, Typical And Atypical
However, it's not some secret code that governs the architecture of the universe, Devlin said. In another study conducted with heart failure and AF patients, TT genotype of GT gene polymorphism was determined as a genetic risk factor in development of AF. Furthermore, in the same study, this polymorphism was found to be an independent risk factor for plasma homocysteine concentrations [ 7 — 9 ]. Hemodynamic changes following sympathetic or parasympathetic activation play an important role in AF triggering.
Since myocardial hypertrophy is present in patients with hypertrophic cardiomyopathy, the left ventricular space is small in these patients. Thus, a decrease occurs in venous conversion and intravascular volume. As a result of this, in the patients with hypertrophic cardiomyopathy, low heart debit and various symptoms arise.
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Endothelin 2, which constricts the systemic vessels, protects venous return and prevents hypertension that may develop. Acute hypertension causes an increase in sympathetic nerve activity. Hypertension can occur in hypertrophic cardiomyopathy. A vasoconstrictor may show protective effect against AF in hypertrophic cardiomyopathy. Proximal AF is more common in hypertrophic cardiomyopathy than in other structural heart diseases.
This monogenic disorder is a disorder affecting left ventricular hypertrophy in patients with hypertrophic cardiomyopathy.
These disorders result from mutations in genes encoding the sarcomeric proteins. Endothelin 2 gene is localized on chromosome 1p It has been suggested that there is a significant relationship between hemodynamic changes and polymorphisms occurring in endothelin 2 gene in patients with essential hypertension. The functional role of endothelin 2 AG gene polymorphism is not known precisely. Thus, endothelin 2 transcription and translation may be affected in the endothelin 2 AG gene polymorphism.
Differences in A allele frequencies are observed in studies with different populations. Endothelin 2 AG gene polymorphism plays a protective role for A allelic cardiovascular diseases, but this allele may trigger AF development in hypertrophic cardiomyopathic patients.
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It is presented primer sequences that used to determine Endothelin 2 AG gene polymorphism in Table 4. AF can also occur when there is or no structural heart disease. Most of the foci that cause AF are at the site where combine the cardiomyocytes and vascular smooth muscle cells are located near the pulmonary venules.
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Connexins Cx are gap junction proteins and play an important role in direct cell-cell interactions in the majority of the tissues of the body in electrical conduction in the heart. It is known that there are 20 different Cxs in humans, and each Cxs create channels with different characteristics and specific expression patterns. The polymorphisms occur in gap junction channels and in Cx proteins that play a role in action potential spread. Variants that occur in genes encoding variants that occur in genes encoding Cx40 and Cx37 that contribute to pulmonary vein-arrhythmogenic affect gene expression and function.
Cx40 and Cx37 that contribute to pulmonary vein-arrhythmogenic affect gene expression and function. Variants that occur in genes encoding Cx40 and Cx37 that contribute to pulmonary vein-arrhythmia affect gene expression and function. The Cx40 gene is encoded by GJA5 and is expressed in endothelial cells, coronary vascular smooth muscle cells, atrial cardiomyocytes and cardiac conduction systems.
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Somatic mutations in the Cx40 gene have also been associated with idiopathic AF. The Cx43 gene is also encoded by GJA1 and is expressed by ventricular, atrial cardiomyocytes, vascular smooth muscle cells, endothelial cells, monocytes and macrophages. Other genes and polymorphisms associated with polymorphisms in the CX43 gene have also been reported to be effective in the development of AF.
Thus, they are important in the regulation of local inflammation. Systemic and local inflammation may play a role in the development of AF before or after surgery in some cases. As a result, channel conductivity and permeability change. Due to the effect of this polymorphism on monocyte adhesion, sensitivity to non-structural AF may change [ 11 — 13 ].
Warfarin, an oral anticoagulant, is used in the correction of various thromboembolitic disorders such as prosthetic heart valves, deep vein thrombosis and pulmonary embolism. Thromboembolism or bleeding may develop as a result of inadequate or excessive intake of warfarin. Discomforts such as stroke and systemic thromboembolism can be reduced with anticoagulant treatments.
Factors such as age, body size, environment, interacting drugs and gene polymorphisms are effective at warfarin dose requirements.
Stable warfarin dose is affected by gene polymorphisms such as single nucleotide gene polymorphism. These polymorphisms play a role in the modulation of warfarin pharmacodynamics and pharmacokinetics. Gamma carbon carboxylation occurs on gamma glutamic acids. Gamma-glutamyl carboxylase GGCX found in the endoplasmic reticulum membrane oxidizes vitamin K-2,3 epoxite reduced vitamin K.
GGCX catalyzes the biosynthesis of vitamin K-dependent clotting factors. Thus, this enzyme affects warfarin metabolism. Warfarin metabolism, one of the most frequently used anticoagulants in clinical therapy, is affected by the GGCX enzyme. GGCX is a gene that plays an important role in the individual differences of warfarin response. Warfarin is a common anticoagulant that a narrow therapeutic range. Genetic factors that play an important role in warfarin dose requirements include GGCX gene polymorphisms. GGCX gene that consisted of exon is located on human chromosome 2p It has been reported that there is a relationship between polymorphisms occurring in the GGCX gene and warfarin dose variability.
In Caucasians and African Americans, there is a significant relationship between GGCX rs microsatellite DNA repeats gene polymorphism in intron 6 and high warfarin dose requirements. In Japanese and Chinese patients, a significant relationship was determined between this polymorphism and high warfarin dose requirements.
In contrast, in Caucasians or African Americans, this gene polymorphism was found not to be associated with warfarin dose. It is presented primer sequences that used to determine GGCX rs, rs gene polymorphisms in Table 6.
In conclusion, gene polymorphisms encoding ion channels are very important in AF pathogenesis. Identification of these polymorphisms will elucidate the multigenic mechanism of AF predisposition [ 16 ]. Differences in populations due to myocardial membrane stability, conduction routes or genetic polymorphisms are important factors in predisposing to AF development.
In recent association studies, gene polymorphisms found on chromosomes 4q25, 16q22 and 1q21 have been identified as genetic risk factors for AF development.