Cardiomiopatia hipertrófica felina

A Cardiomiopatia Hipertrófica (CMH) é uma doença é a doença cardíaca primária mais comum em gatos causada por uma mutação genética autossómica de dominância incompleta com apresentações clínicas variadas que apresenta uma grande dispersão mundial e racial. O carácter hereditário desta doença cardíaca resulta de uma mutação genética autossómica dominante com penetração incompleta, sendo mais exuberante em situações de homozigotia. A mutação mais comum ocorre em genes que codificam para a Proteína C3 de Ligação à Miosina, com alterações estruturais do mesmo e consequente hipertrofia concêntrica parcial ou total do ventrículo esquerdo. Com o aumento do septo interventricular, dos músculos papilares e/ou da parede do ventrículo esquerdo, ocorre comprometimento tanto do enchimento ventricular como do seu relaxamento, o que por sua vez contribui para a progressão da hipertrofia. A diminuição da câmara cardíaca, a diminuição do débito cardíaco, o aumento compensatório do ritmo, o aumento da pressão de enchimento diastólico e o aumento do átrio esquerdo predispõem para uma insuficiência cardíaca congestiva, formação trombos e até morte súbita. A avaliação clínica de um gato com suspeita de Cardiomiopatia Hipertrófica deve ser exaustiva, mesmo que o diagnóstico definitivo apenas possa ser confirmado através de ecocardiografia e de métodos de biologia molecular no sentido de identificar a mutação genética. A ecocardiografia pode ainda ser útil para direcionar a terapêutica em função do grau de hipertrofia estabelecer prognóstico. Atualmente, em medicina humana, existem outras formas de terapêutica, como o novo MYK 461, que se revelam bastante promissores.The Hypertrophic Cardiomyopathy is the heart disease more common in cats caused by a genetic autossomic mutation with imcomplete penetrance, having several clinic findings worldwide and inbreed. This disease assumes an hereditary character associated with a genetic mutation autossomic dominant with incomplete penetrance, being more exuberant in homozigotic. It’s a common mutation in genes that codify for the Myosin Binding Protein C (MYBPC3), with structural alteration of itself and leading to the partial or total concentric hypertrophy os left ventricule. With the increase of the interventricular septum and/or papillary muscles and/or left ventricle hall there is a compromise of the ventricular filling and it’s relaxation, which in other hand contributes to the progression of the hypertrophy. The decrease of the cardiac chamber, the decrease of cardiac output, the compensatory increase of rhythm, the increase of pressure in diastolic filling and the increase of the left atrium predispose to congestive heart failure and even sudden death. Cats clinical evaluation under the suspect of Hypertrophic Cardiomyopathy should be exhaustive, even if the definite diagnostic can only be confirmed throght Ultrasound and bio molecular methods looking for identification of genetic mutations. Ultrasound can also be useful to direct the therapeutics accordingly to the level of Hypertrophy, and better prognostics. Nowadays, there are other new therapeutic drugs, like MYK 461, that are showing promissing results

Optimal Quadratic Programming Algorithms

Quadratic programming (QP) is one technique that allows for the optimization of a quadratic function in several variables in the presence of linear constraints. This title presents various algorithms for solving large QP problems. It is suitable as an introductory text on quadratic programming for graduate students and researcher

Technical Aspects of New Concentrating Solar Thermomechanic Conversion

The article concerns technical aspects of new concentrating solar thermo-mechanic conversion from the point of view of automated control algorithms of solar thermal motor working on a principle of modified Clausius-Rankin's thermal circulation. On the basis of the proposed algorithms for controlling of thermodynamic processes of the functional model of the solar thermal motor, which uses internal-system absorption of incoming heat radiation, double-step steam generation and regeneration of out coming heat, the design and the testing of controlling single-chip microprocessor electronics with specially designed software was executed

Respiratory parameters of permeabilised H9c2 cells treated with nothing (white bars), DMSO (dark grey bars), quercetin (25 μM) (grey bars) or DHS (1 μM) (light grey bars) as measured by high resolution respirometry (protocols C & D).

<p>Cells were incubated under normoxia (plain bars) or hypoxia (hatched bars) for 3 h, followed by oxygraphy with digitonin for permeabilisation. <b>(a)</b> Shows the differences in relative rate of respiration on malate + palmitate + ADP (relative to maximum respiratory rate of control permeabilised cells) prior to and following addition of cytochrome c, hence acting as a proxy for cytochrome c loss from mitochondria. <b>(b)</b> Shows the respiration of cells treated with DMSO, quercetin or DHS (following normoxia or hypoxia) on various substrates: Complex I respiration; “Complex I” (malate + palmitate + ADP + cytochrome c + pyruvate + glutamate), uncoupled respiration under complex I; “Complex I uncoupled” (“Complex I” + oligomycin +FCCP), uncoupled respiration under complex I and complex II; “Respiratory Chain” (“Complex I uncoupled” + Succ) and uncoupled complex II respiration; “Complex II uncoupled” (“Respiratory Chain” + Rotenone). Statistically significant differences from vehicle-control were denoted by * (p < 0.05), ** (p < 0.01) and *** (p < 0.001) and from untreated control by † (p < 0.05), †† (p < 0.01) and ††† (p < 0.001).</p

On the causes and consequences of the uncoupler-like effects of quercetin and dehydrosilybin in H9c2 cells - Fig 4

<p>Loss of mitochondrial membrane potential, as indicated by ratiometric fluorimetry with JC-1 following treatment with DHS <b>(a)</b> and quercetin <b>(b)</b>. Cells were incubated with JC-1 for 1 h under hypoxia or normoxia, and subsequently measurements taken immediately. The solid line represents normoxia treated cells. The dashed line represents hypoxia treated cells.</p