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Example sentences for: cmh
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is expressed in skeletal muscle, with a less abundant ~7 kb transcript expressed in both skeletal and cardiac muscle [ 8 ] . Whereas tropomodulins or the Arp 2/3 complex cap the pointed end of actin filaments, the barbed end can be capped by CapZ, α, β, and γ adducins as well as gelsolin [ 9 10 11 ] . Control of thin filament length is critical for maintaining proper sarcomere function and length [ 12 ] . Inhibition of Tmod1's capping activity - either by using an antibody to its C-terminal end or by decreasing expression using an antisense Tmod1 transcript - results in elongated thin filaments and decreased cardiac contractility [ 13 14 ] . Tmod1 overexpression in rat cardiomyocytes causes shortening of the thin filaments and sarcomere disorganization, resulting in myofibril degeneration [ 14 ] . Likewise, mice overexpressing TMOD1 in the heart show disrupted sarcomere organization with shortened thin filaments, leading to myofibril degeneration and dilated cardiomyopathy [ 15 ] . Recently, Littlefield and colleagues showed that overexpression of GFP-Tmod1 in chick cardiac myocytes results in shortening of thin filaments; the authors proposed that excess Tmod1 decreases the affinity between actin monomers and pointed ends, leading to monomer dissociation and filament shortening [ 42 ] . Mutations in many proteins making up the cardiac sarcomere have been shown to cause cardiac hypertrophy [ 16 17 18 19 ] :mutations in the TPM1 gene, for example, cause type 3 familial hypertrophic cardiomyopathy (CMH3), and a transgenic mouse expressing a CMH3 mutation develops ventricular myocyte disarray and hypertrophy [ 20 ] . Mutations in myosin heavy chain 7 are estimated to account for 40-50% of the cases of hypertrophic cardiomyopathy [ 21 ] .
Tidal volume was reduced to maintain peak airway pressures of less than 40 cmH 2 O. Respiratory rate was adjusted to maintain a pH of more than 7.30.
The results presented here, which demonstrate a lack of impact on splanchnic blood flow when PEEP is not accompanied by decreased cardiac output, corroborate those from animal studies [ 4 13 ] and from the recent human study conducted by Kiefer and coworkers [ 9 ] . The lack of change in pH i at PEEP opt (11 cmH 2 O) is in agreement with our current understanding that PEEP at 10 cmH 2 O has a limited effect on splanchnic blood flow.
We determined H 2 O displacement lung volumes at total lung capacity (25 cmH 2 O airway pressure) as the simplest measure to document the hyperexpansion characteristic of emphysema in the elastase-treated animals.
The highest PEEP value applied was 17 cmH 2 O. Static compliance improved slightly at PEEP opt , but this did not achieve statistical significance ( P = 0.84; Table 2).
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