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Focal adhesion kinase (FAK) is a nonreceptor tyrosine kinase that plays an important role in integrin-mediated signal transduction. To explore the role and mechanisms of FAK in cardiac development, we inactivated FAK in embryonic cardiomyocytes by crossing the floxed FAK mice with myosin light chain-2a (MLC2a) Cre mice, which expressed Cre as early as embryonic day 9.5 in the heart. The majority of conditional FAK knockout mice generated from MLC2a-Cre (CFKO-2a) died in the embryonic stage with thin ventricular wall and ventricular septal defects. A small fraction of CFKO-2a mice survived to adulthood with spontaneous eccentric right ventricle hypertrophy. Transmission electron microscopy analysis displayed swelling in the rough endoplasmic reticulum in CFKO-2a embryonic cardiomyocytes. We found that decreased cell proliferation, but not increased cell apoptosis or differentiation, is the reason for the thin ventricular wall in CFKO-2a mice. Microarray analysis suggests that myocyte enhancer factor 2a (MEF2a) can be regulated by FAK and that inactivation of FAK in the embryonic heart compromised MEF2a expression. Last, we found that Src, but not PI3K, is important in mediating signal transduction for the regulation of MEF2a by FAK. Together, these results identified the role and mechanisms of FAK in embryonic cardiac development. [ABSTRACT FROM AUTHOR]

Focal adhesion kinase (FAK) is a cytoplasmic tyrosine kinase that plays a major role in integrin signaling pathways. Although cardiovascular defects were observed in FAK total KO mice, the embryonic lethality prevented investigation of FAK function in the hearts of adult animals. To circumvent these problems, we created mice in which FAK is selectively inactivated in cardiomyocytes (CFKO mice). We found that CFKO mice develop eccentric cardiac hypertrophy (normal LV wall thickness and increased left chamber dimension) upon stimulation with angiotensin II or pressure overload by transverse aortic constriction as measured by echocardiography. We also found increased heart/body weight ratios, elevated markers of cardiac hypertrophy, multifocal interstitial fibrosis, and increased collagen I and VI expression in CFKO mice compared with control littermates. Spontaneous cardiac chamber dilation and increased expression of hypertrophy markers were found in the older CFKO mice. Analysis of cardiomyocytes isolated from CFKO mice showed increased length but not width. The myocardium of CFKO mice exhibited disorganized myofibrils with increased nonmyofibrillar space filled with swelled mitochondria. Last, decreased tyrosine phosphorylation of FAK substrates p130Cas and paxillin were observed in CFKO mice compared with the control littermates. Together, these results provide strong evidence for a role of FAK in the regulation of heart hypertrophy in vivo. [ABSTRACT FROM AUTHOR]

Objective--To determine electrocardiographic parameters in healthy llamas and alpacas. Animals--23 llamas and 12 alpacas. Procedure--Electrocardiography was performed in nonsedated standing llamas and alpacas by use of multiple simultaneous lead recording (bipolar limb, unipolar augmented limb, and unipolar precordial leads). Results--Common features of ECGs of llamas and alpacas included low voltage of QRS complexes, variable morphology of QRS complexes among camelids, and mean depolarization vectors (mean electrical axes) that were directed dorsocranially and to the right. Durations of the QT interval and ST segment were negatively correlated with heart rate. Conclusions and Clinical Relevance--ECGs of acceptable quality can be consistently recorded in nonsedated standing llamas and alpacas. Features of ECGs in llamas and alpacas are similar to those of other ruminants. Changes in the morphology of the QRS complexes and mean electrical axis are unlikely to be sensitive indicators of ventricular enlargement in llamas and alpacas. (Am J Vet Res 2004;65:1719-1723). [ABSTRACT FROM AUTHOR]

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A response by Kathleen R. Mullen and colleagues to a letter to the editor on their article reaging a horse that was examined because of decreased appetite, diarrhea, and weight loss, published in a previous issue of the journal is presented.

Many diseases have been linked with birth seasonality, and these fall into four main categories: mental, cardiovascular, respiratory and women's reproductive health conditions. Informatics methods are needed to uncover seasonally varying infectious diseases that may be responsible for the increased birth month-dependent disease risk observed. We have developed a method to link seasonal infectious disease data from the USA to birth month dependent disease data from humans and canines. We also include seasonal air pollution and climate data to determine the seasonal factors most likely involved in the response. We test our method with osteosarcoma, a rare bone cancer. We found the Lyme disease incidence was the most strongly correlated significant factor in explaining the birth month-osteosarcoma disease pattern (R=0.418, p=2.80X10-23), and this was true across all populations observed: canines, pediatric, and adult populations., (©2021 AMIA - All rights reserved.)

Pacemakers were implanted in 4 client-owned female dogs which had persistent atrial standstill. Three dogs were alive after 14 to 39 months and 1 dog was euthanized after 10.5 years. This report demonstrates that some dogs with persistent atrial standstill can survive for extended time periods.