Example sentences for: sarcomere

How can you use “sarcomere” in a sentence? Here are some example sentences to help you improve your vocabulary:

  • When stimulation was 10 Hz for 10 s, at 35°C, there was a staircase potentiation (P t */P t > 1) which was evident at all sarcomere lengths studied (range = 2.4 μm - 3.6 μm).

  • The first (P t ) and last (P t *) contraction in each series were collected (4000 Hz analogue to digital conversion) for assessment of the effects of repetitive stimulation (P t */P t ). The sarcomere length was always the same after the 10 s of stimulation as it had been prior to the stimulation.

  • It is interesting that the twitch contraction after a brief tetanic contraction at 22°C in our experiments demonstrated potentiation when the response was measured at short sarcomere lengths, and depression when the response was measured at long sarcomere lengths.

  • The data in Figure 1would center around the line representing the theoretical length-tension relationship if sarcomere length for each contraction was corrected by subtracting 0.19 μm.

  • 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 ] .


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