Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “THINNESS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources
PubMed1981

Phosphorylation of the calcium ion-regulated thin filaments from vascular smooth muscle. A new regulatory mechanism?

The thin filaments of vascular smooth muscle (pig aorta) contain a Ca2+-sensitive regulatory system that resembles troponin-tropomyosin [Marston, Trevett & Walters (1980) Biochem. J. 185, 355-365]. Our thin-filament preparations also contain enzymes that phosphorylate and dephosphorylate a specific protein. Initial rate of phosphorylation was 0.42 +/- 0.10 (95% confidence limits) mumol of Pi/min per g of thin filaments; half-maximal incorporation was obtained in 4 1/2 min, and a maximum of 1.8 +/- 0.1 mumol of Pi/g of thin filaments was incorporated after 40 min (conditions: 1 mM-MgATP, 60 mM-MgATP, 60 mM-KCl, 10 mM-imidazole, pH 7.0, 5 mM-MgCl2, 10 mM-NaN3, 0.5 mM-dithiothreitol, 0.1 mM-CaCl2, 25 degrees C). On gel electrophoresis in polyacrylamide (4-30% gradient)/0.25% sodium dodecyl sulphate gel over 75% of protein-bound phosphate was in a single protein of mol.wt. 21000. On electrophoresis in polyacrylamide (8%)/6 M-urea (pH 8.6) gel the phosphoprotein remained at the origin. Phosphorylation was associated with an increase in the concentration of high-affinity (K congruent to 10(6) M-1) Ca2+-binding sites from 0.8-1.5 to 6.3 mumol of Ca2+/g of thin filaments. Phosphorylation also changed the regulatory properties of the skeletal-muscle myosin-aorta thin-filament MgATPase; maximum activity was unaltered, but the phosphorylated thin filaments required only 0.36 microM-Ca2+ for half-activation compared with 2.7 microM-Ca2+ for unphosphorylated thin filaments. The possible regulatory role of thin-filament phosphorylation is discussed.

Actomyosin↗
PubMed2005

Mini-thin filaments regulated by troponin-tropomyosin.

Striated muscle thin filaments contain hundreds of actin monomers and scores of troponins and tropomyosins. To study the cooperative mechanism of thin filaments, "mini-thin filaments" were generated by isolating particles nearly matching the minimal structural repeat of thin filaments: a double helix of actin subunits with each strand approximately seven actins long and spanned by a troponin-tropomyosin complex. One end of the particles was capped by a gelsolin (segment 1-3)-TnT fusion protein (substituting for normal TnT), and the other end was capped by tropomodulin. EM showed that the particles were 46 +/- 9 nm long, with a knob-like mass attributable to gelsolin at one end. Average actin, tropomyosin, and gelsolin-troponin composition indicated one troponin-tropomyosin attached to each strand of the two-stranded actin filament. The minifilaments thus nearly represent single regulatory units of thin filaments. The myosin S1 MgATPase rate stimulated by the minifilaments was Ca2+-sensitive, indicating that single regulatory length particles are sufficient for regulation. Ca2+ bound cooperatively to cardiac TnC in conventional thin filaments but noncooperatively to cardiac TnC in minifilaments in the absence of myosin. This suggests that thin filament Ca2+-binding cooperativity reflects indirect troponin-troponin interactions along the long axis of conventional filaments, which do not occur in minifilaments. Despite noncooperative Ca2+ binding to minifilaments in the absence of myosin, Ca2+ cooperatively activated the myosin S1-particle ATPase rate. Two-stranded single regulatory units therefore may be sufficient for myosin-mediated Ca2+-binding cooperativity. Functional mini-thin filaments are well suited for biochemical and structural analysis of thin-filament regulation.

Actin Cytoskeleton↗
PubMed1995

Effects of thinning on soil and tree water relations, transpiration and growth in an oak forest (Quercus petraea (Matt.) Liebl.).

To quantify the effects of crown thinning on the water balance and growth of the stand and to analyze the ecophysiological modifications induced by canopy opening on individual tree water relations, we conducted a thinning experiment in a 43-year-old Quercus petraea stand by removing trees from the upper canopy level. Soil water content, rainfall interception, sap flow, leaf water potential and stomatal conductance were monitored for two seasons following thinning. Seasonal time courses of leaf area index (LAI) and girth increment were also measured. Predawn leaf water potential was significantly higher in trees in the thinned stand than in the closed stand, as a consequence of higher relative extractable water in the soil. The improvement in water availability in the thinned stand resulted from decreases in both interception and transpiration. From Year 1 to Year 2, an increase in transpiration was observed in the thinned stand without any modification in LAI, whereas changes in transpiration in the closed stand were accompanied by variations in LAI. The different behaviors of the closed and open canopies were interpreted in terms of coupling to the atmosphere. Thinning increased inter-tree variability in sap flow density, which was closely related to a leaf area competition index. Stomatal conductance varied little inside the crown and differences in stomatal conductance between the treatments appeared only during a water shortage and affected mainly the closed stand. Thinning enhanced tree growth as a result of a longer growing period due to the absence of summer drought and higher rates of growth. Suppressed and dominant trees benefited more from thinning than trees in the codominant classes.

Journal Article↗
PubMed2005

A thin film nitinol heart valve.

In order to create a less thrombogenic heart valve with improved longevity, a prosthetic heart valve was developed using thin film nitinol (NiTi). A "butterfly" valve was constructed using a single, elliptical piece of thin film NiTi and a scaffold made from Teflon tubing and NiTi wire. Flow tests and pressure readings across the valve were performed in vitro in a pulsatile flow loop. Bio-corrosion experiments were conducted on untreated and passivated thin film nitinol. To determine the material's in vivo biocompatibility, thin film nitinol was implanted in pigs using stents covered with thin film NiTi. Flow rates and pressure tracings across the valve were comparable to those through a commercially available 19 mm Perimount Edwards tissue valve. No signs of corrosion were present on thin film nitinol samples after immersion in Hank's solution for one month. Finally, organ and tissue samples explanted from four pigs at 2, 3, 4, and 6 weeks after thin film NiTi implantation appeared without disease, and the thin film nitinol itself was without thrombus formation. Although long term testing is still necessary, thin film NiTi may be very well suited for use in artificial heart valves.

Alloys↗
PubMed1992

In vitro perfusion of chinchilla thin limb segments: segmentation and osmotic water permeability.

The thin limb segments of the long loop of Henle are thought to play important roles in the urinary concentrating mechanism. In this study, we present new approaches to the identification, dissection, and in vitro perfusion of individual thin limb segments from all levels of the chinchilla renal medulla, including the deepest portions of the papilla. We have applied these techniques to the investigation of the osmotic water permeability along the chinchilla long loop of Henle. The results demonstrate that the osmotic water permeability of the thin descending limb is not uniformly high along its length, as previously thought, but that the distal 20% of the long-loop descending limb has a very low water permeability (approximately 50 microns/s). The transition to the low water permeability region of the thin descending limb is accompanied by a relatively abrupt change in morphology (increased cellularity and decreased diameter) that is readily perceptible in the perfused segments and even in the dissection dish. In contrast, the upper part of the chinchilla long-loop thin descending limb had an extremely high osmotic water permeability (greater than 2,000 microns/s) as observed in other species. Thin ascending limbs from deep in the inner medulla had water permeabilities that were indistinguishable from zero, as previously found in thin ascending limbs from near the inner-outer medullary junction. The presence of a low-water-permeability portion of the long-loop thin descending limb in chinchilla may have important implications with regard to the inner medullary concentrating process. A relatively low osmotic water permeability (397 microns/s) was also found in the deep inner medullary portion of the thin descending limb from the rat.

Animals↗
PubMed2004

Thin-filament-based modulation of contractile performance in human heart failure.

BACKGROUND: The contribution of the sarcomere's thin filament to the contractile dysfunction of human cardiomyopathy is not well understood. METHODS AND RESULTS: We have developed techniques to isolate and functionally characterize intact (native) thin filaments obtained from failing and nonfailing human ventricular tissue. By use of in vitro motility and force assays, native thin filaments from failing ventricular tissue exhibited a 19% increase in maximal velocity but a 27% decrease in maximal contractile force compared with nonfailing myocardium. Native thin filaments isolated from human myocardium after left ventricular assist device support demonstrated a 37% increase in contractile force. Dephosphorylation of failing native thin filaments resulted in a near-normalization of thin-filament function, implying a phosphorylation-mediated mechanism. Tissue expression of the protein kinase C isoforms alpha, beta1, and beta2 was increased in failing human myocardium and reduced after left ventricular assist device support. CONCLUSIONS: These novel findings demonstrate that (1) the thin filament is a key modulator of contractile performance in the failing human heart, (2) thin-filament function is restored to near normal levels after LVAD support, and (3) the alteration of thin-filament function in failing human myocardium is mediated through phosphorylation, most likely through activation of protein kinase C.

Actin Cytoskeleton↗
PubMed1991

Thin filament changes during in vivo rat heart development.

Developmental differences in myocardial performance are known to exist. It is likely that the profile of protein isoforms present on the developing thin filament contributes to these observed differences. We have prepared thin filaments from developing and mature rat hearts by using an immunoprecipitation procedure developed in our laboratory. Analysis of these isolated thin filaments by Western immunoblots and two-dimensional gel electrophoresis demonstrates troponin I and troponin T isoform switching on the developing thin filament. Troponin I isoform switching begins by embryonic d 18 and is complete before the 3rd postnatal wk. Troponin T isoform switching begins between embryonic d 18 and birth and is complete between the 2nd and 3rd postnatal wk. The degree of phosphorylation of tropomyosin in thin filaments appears to be developmentally regulated, decreasing with advancing age. Nonmuscle isoforms of tropomyosin are also detectable in thin filaments from developing and mature rat hearts. These phenomena (troponin isoform switching, the degree of phosphorylation of tropomyosin, and the presence of nonmuscle isoforms of tropomyosin on cardiac thin filaments) likely play a role in the function of immature thin filaments and in the assembly of mature thin filaments.

Actin Cytoskeleton↗
PubMed2006

Thin glomerular basement membrane nephropathy: incidence in 3471 consecutive renal biopsies examined by electron microscopy.

CONTEXT: Thin glomerular basement membrane (GBM) nephropathy is often equated with benign familial hematuria, although it may occur sporadically and may not always be benign. Thin GBM nephropathy is reported to occur in at least 1% of the population, although its reported incidence varies considerably in different studies because there are presently no uniform criteria for its diagnosis by electron microscopy (EM). OBJECTIVE: To determine the incidence of thin GBM nephropathy in a large sample of renal biopsies using a basic methodology that can easily be applied in any diagnostic EM laboratory. DESIGN: Direct measurements of GBM thickness were made from electron micrographs at 3 specified points along each of 10 randomly selected glomerular capillaries to determine an average GBM thickness for each of 50 males and 50 females, ages 9 to 80 years, with minimal-change nephropathy or acute interstitial nephritis, without hematuria. The means of the average GBM thickness values were 330 +/- 50 (SD) nm in the males and 305 +/- 45 nm in the females; normal ranges for each sex were defined as being within 2 SD of these means. The average GBM thickness was then similarly determined for renal biopsies with suspected thin GBMs examined from January 2000 to December 2004; a total of 3471 renal biopsies were examined by EM during this period. SETTING: Academic medical center renal pathology/EM laboratory. RESULTS: Excluding biopsies with immunoglobulin A nephropathy, which is known to be frequently associated with thin GBMs, and biopsies with Alport syndrome, 67 biopsies (1.9% of total) had an average GBM thickness below the sex-specific normal range. Of these, 37 biopsies were performed specifically because of hematuria and had an average GBM thickness of 121 to 215 nm (mean, 185 +/- 20 nm). The remaining 30 (0.9%) biopsies, with average GBM thicknesses of 143 to 227 nm (mean, 190 +/- 20 nm), represent cases of incidentally discovered thin GBM nephropathy. CONCLUSIONS: Based on the frequency of incidentally discovered cases and taking into account excluded cases and biopsies (eg, with diabetic nephropathy) in which diagnosis of incidental thin GBM nephropathy by EM is not possible, the incidence of thin GBM nephropathy in our population is estimated to be between 1% and 2%. Diseases most often associated with incidental thin GBM nephropathy were focal segmental glomerulosclerosis (10 cases) and minimal-change nephropathy (5 cases).

Acute Disease↗
PubMed1987

Activation of smooth muscle myosin Mg2+-ATPase by native thin filaments and actin/tropomyosin.

Application of the myosin competition test (Lehman, W., and Szent-Györgyi, A. G. (1975) J. Gen. Physiol. 66, 1-30) to chicken gizzard actomyosin indicated that this smooth muscle contains a thin filament-linked regulatory mechanism. Chicken gizzard thin filaments, isolated as described previously (Marston, S. B., and Lehman, W. (1985) Biochem. J. 231, 517-522), consisted almost exclusively of actin, tropomyosin, caldesmon, and an unidentified 32-kilodalton polypeptide in molar ratios of 1:1/6:1/26:1/17, respectively. When reconstituted with phosphorylated gizzard myosin, these thin filaments conferred Ca2+ sensitivity (67.8 +/- 2.1%; n = 5) on the myosin Mg2+-ATPase. On the other hand, no Ca2+ sensitivity of the myosin Mg2+-ATPase was observed when purified gizzard actin or actin plus tropomyosin was reconstituted with phosphorylated gizzard myosin. Native thin filaments were rendered essentially free of caldesmon and the 32-kilodalton polypeptide by extraction with 25 mM MgCl2. When reconstituted with phosphorylated gizzard myosin, caldesmon-free thin filaments and native thin filaments exhibited approximately the same Ca2+ sensitivity (45.1 and 42.7%, respectively). The observed Ca2+ sensitivity appears, therefore, not to be due to caldesmon. Only trace amounts of two Ca2+-binding proteins could be detected in native thin filaments. These were identified as calmodulin (present at a molar ratio to actin of 1:733) and the 20-kilodalton light chain of myosin (present at a molar ratio to actin of 1:270). The Ca2+ sensitivity observed in an in vitro system reconstituted from gizzard thin filaments and either skeletal myosin or phosphorylated gizzard myosin is due, therefore, to calmodulin and/or an unidentified minor protein component of the thin filaments which may be an actin-binding protein involved in regulating actin filament structure in a Ca2+-dependent manner.

Actins↗
PubMed2000

Reflection and absorption of millimeter waves by thin absorbing films.

Reflection, transmission, and absorption of mm-waves by thin absorbing films were determined at two therapeutic frequencies: 42. 25 and 53.57 GHz. Thin filter strips saturated with distilled water or an alcohol-water solution were used as absorbing samples of different thicknesses. The dependence of the power reflection coefficient R(d) on film thickness (d) was not monotonic. R(d) passed through a pronounced maximum before reaching its steady-state level [R(infinity)]. Similarly, absorption, A(d), passed two maximums with one minimum between them, before reaching its steady-state level [A(infinity)]. At 42.25 GHz, A(d) was compared with absorption in a semi-infinite water medium at a depth d. When d < 0.3 mm, absorption by the film increased: at d = 0.1 mm the absorption ratio for the thin layer sample and the semi-infinite medium was 3.2, while at d = 0.05 mm it increased up to 5.8. Calculations based on Fresnel equations for flat thin layers adequately described the dependence of the reflection, transmission, and absorption on d and allowed the determination of the refractive index (n), dielectric constant (epsilon), and penetration depth (delta) of the absorbing medium for various frequencies. For water samples, epsilon was found to be 12.4-19.3j, delta = 0.49 mm at 42.25 GHz, and epsilon = 9.0-19.5j, delta = 0.36 mm at 53.57 GHz. The calculated power density distribution within the film was strongly dependent on d. The measurements and calculations have shown that the reflection and absorption of mm-waves by thin absorbing layers can significantly differ from the reflection and absorption in similar semi-infinite media. The difference in reflection, absorption, and power density distribution in films, as compared to semi-infinite media, are caused by multiple internal reflections from the film boundaries. That is why, when using thin phantoms and thin biological samples, the specifics of the interaction of mm-waves with thin films should be taken into account.

Absorption↗
PubMed1981

Freeze-fracture studies on the thin limbs of Henle's loop in Psammomys obesus.

The thin limbs of short and long loops of Henle of the desert rodent Psammomys obesus were studied by freeze-fracture techniques. Intercellular junctions and internal membrane characteristics of thin-limb epithelia are of interest with regard to the high urine-concentrating capacity of this animal. The epithelium of the descending thin limbs of short loops is remarkably undifferentiated and equipped with multistrand tight junctions. In the descending thin limb of long loops, two segments are to be distinguished. The upper parts are characterized by an extensive cellular interdigitation and single-strand tight junctions. Thus, the paracellular pathways are prominent from two aspects: the junctional belt is elongated by interdigitation, and its apico-basal depth is shallow. The transition from the upper to the lower part appears to be abrupt, as indicated by the change in intramembrane particle density. The lower parts are characterized by a noninterdigitating epithelium with junctions consisting of few, but always more than two, strands. In addition, this thin-limb segment is characterized by regularly distributed infoldings of the basal cell membrane. The ascending thin limbs are established by an interdigitation epithelium, with junctions generally consisting of one strand. Once again, the elongated junctional belt is shallow. This study presents further evidence that remarkable species difference occur among thin-limb epithelia, especially concerning the descending thin limbs of long loops. Those differences may well explain discrepant functional findings concerning the transport properties of this segment in various species.

Animals↗
PubMed1998

Regional difference in epidermal thinning after skin denervation.

Denervation of skin has a profound influence on epidermis; epidermal thinning was a consistent finding in rats. However, it is not clear whether the degree of epidermal thinning was similar in the region receiving the same innervation. In mice, how early epidermal nerves were degenerated after nerve injury remained unknown. To address these issues, we transected the sciatic nerve in mice and compared the changes of epidermal thickness in different areas of the hind foot skin. Epidermal nerves degenerated within 48 h after nerve transection, similar to what was observed in rats. Seven days after nerve transection, there was differential thinning of epidermis. The interpad area, in the center of the sciatic nerve-innervated region, exhibited the most profound degree of epidermal thinning (34.6 +/- 3.1 vs 47.8 +/- 2.4 microns, P < 0.01). The heel area, in the periphery of the sciatic nerve-innervated zone, did not show significant thinning of epidermis after denervation (37.3 +/- 4.8 vs 41.5 +/- 5.1 microns, P > 0.05). The degree of epidermal thinning after denervation in the pad area was the intermediate one: with 98.8 +/- 4.8 vs 120.1 +/- 7.3 microns, P < 0.02, in the rete pegs, and 51.1 +/- 4.1 vs 62.1 +/- 6.0 microns, P < 0.02, in the dermal papilla. The differential thinning was obvious when the thickness of the denervated epidermis was normalized to that of the control epidermis with the ratios of 0.73 +/- 0.03 in the interpad area, 0.83 +/- 0.04 in the rete peg, 0.85 +/- 0.05 in the dermal papilla, and 0.92 +/- 0.05 in the heel. Epidermal thinning was reversed by reinnervation of the epidermis after sciatic nerve crush (41.5 +/- 1.5 vs 45.0 +/- 2.0 microns in the interpad area, P > 0.05). These findings suggest that sensory nerves exhibit trophic influences on the epidermis presumably through the effects of diffusible factors.

Animals↗
PubMed1999

Isolation, electron microscopic imaging, and 3-D visualization of native cardiac thin myofilaments.

An increasing number of cardiac diseases are currently pinpointed to reside at the level of the thin myofilaments (e.g., cardiomyopathies, reperfusion injury). Hence the aim of our study was to develop a new method for the isolation of mammalian thin myofilaments suitable for subsequent high-resolution electron microscopic imaging. Native cardiac thin myofilaments were extracted from glycerinated porcine myocardial tissue in the presence of protease inhibitors. Separation of thick and thin myofilaments was achieved by addition of ATP and several centrifugation steps. Negative staining and subsequent conventional and scanning transmission electron microscopy (STEM) of thin myofilaments permitted visualization of molecular details; unlike conventional preparations of thin myofilaments, our method reveals the F-actin moiety and allows direct recognition of thin myofilament-associated porcine cardiac troponin complexes. They appear as "bulges" at regular intervals of approximately 36 nm along the actin filaments. Protein analysis using SDS-polyacrylamide gel electrophoresis revealed that only approximately 20% troponin I was lost during the isolation procedure. In a further step, 3-D helical reconstructions were calculated using STEM dark-field images. These 3-D reconstructions will allow further characterization of molecular details, and they will be useful for directly visualizing molecular alterations related to diseased cardiac thin myofilaments (e.g., reperfusion injury, alterations of Ca2+-mediated tropomyosin switch).

Actin Cytoskeleton↗
PubMed2005

Relationship between basal thinning of the interventricular septum and atrioventricular block in patients with cardiac sarcoidosis.

BACKGROUND: Basal thinning of the interventricular septum (IVS) and atrioventricular block (AVB) are characteristic features of cardiac sarcoidosis. Since the conduction system passes along IVS, it has been considered that a close connection exists between basal thinning of IVS and AVB. However, neither the incidence of cases showing basal thinning of IVS nor the relation between it and AVB has been clarified. We thus investigated to elucidate these two issues. METHODS: Thirty-five patients with cardiac sarcoidosis were selected for this study and underwent echocardiographic examination. The wall thickness of IVS was measured at a site 1 cm below the aortic valve inserted point of IVS. Thickness of this site < or = 5 mm was defined as thinning. Twelve-lead and Holter electrocardiograms were obtained to determine the presence/absence and degree of AVB. RESULTS: Basal thinning of IVS was noted in 7 of the 35 patients (20%). AVB was present in 4 of these 7 (57%), and was first degree in 3 (43%) and third degree in one (14%). AVB was not present in 3 patients. Basal thinning of IVS was not apparent in 28 of the 35 patients (80%). AVB was observed in 14 of the 28 patients, 3 had first degree block, 2 had second degree block, and 9 had third degree block. AVB was not observed in 14 of the 28 patients. CONCLUSIONS: These results clarified that basal thinning of IVS is not as common as previously thought in cardiac sarcoidosis, basal thinning of IVS and the presence/absence and degree of AVB are not necessarily correlated.

Adult↗
PubMed2004

Competitive regulation of plant allometry and a generalized model for the plant self-thinning process.

Taking into account the individual growth form (allometry) in a plant population and the effects of intraspecific competition on allometry under the population self-thinning condition, and adopting Ogawa's allometric equation 1/y = 1/axb + 1/c as the expression of complex allometry, the generalized model describing the change mode of r (the self-thinning exponential in the self-thinning equation, log M = K + log N, where M is mean plant mass, K is constant, and N is population density) was constructed. Meanwhile, with reference to the changing process of population density to survival curve type B, the exponential, r, was calculated using the software MATHEMATICA 4.0. The results of the numerical simulation show that (1) the value of the self-thinning exponential, r, is mainly determined by allometric parameters; it is most sensitive to change of b of the three allometric parameters, and a and c take second place; (2) the exponential, r, changes continuously from about -3 to the asymptote -1; the slope of -3/2 is a transient value in the population self-thinning process; (3) it is not a 'law' that the slope of the self-thinning trajectory equals or approaches -3/2, and the long-running dispute in ecological research over whether or not the exponential, r, equals -3/2 is meaningless. So future studies on the plant self-thinning process should focus on investigating how plant neighbor competition affects the phenotypic plasticity of plant individuals, what the relationship between the allometry mode and the self-thinning trajectory of plant population is and, in the light of evolution, how plants have adapted to competition pressure by plastic individual growth.

Mathematical Computing↗
PubMedDate not supplied

Clinical significance of apical thinning after attenuation correction.

BACKGROUND: Apical thinning and other image changes at the apex have been described after attenuation correction of myocardial perfusion single photon emission computed tomography (SPECT) studies, but their clinical significance is unknown. METHODS AND RESULTS: We studied 102 subjects from a multicenter trial of attenuation correction, 46 with angiographic coronary artery disease and 56 normal subjects. We graded the presence and magnitude (on a 4-point scale) of apical thinning (decrease in wall thickness, best assessed in the vertical long-axis view) in both noncorrected and attenuation-corrected images. In attenuation-corrected images, apical thinning of any degree was present in 78% of the abnormal patients and 63% of the normal subjects (P = not significant [NS]). However, moderate or severe apical thinning was present in 30% of the abnormal patients compared with 5% of the normal subjects (relative risk = 2.2, P <.001). In noncorrected images, apical thinning of any degree was present in 87% of the abnormal patients and 71% of the normal subjects (P = NS). However, moderate or severe apical thinning was present in 28% of the abnormal patients compared with 4% of the normal subjects (relative risk = 2.3, P <.001). CONCLUSION: The presence of mild apical thinning is common in both noncorrected and attenuation-corrected SPECT images and does not imply coronary artery disease. Moderate or severe apical thinning is 7 times more common in patients than in normal subjects, but it is relatively uncommon and thus is not a generally useful clinical tool.

Coronary Angiography↗
PubMed2005

Remote control of A-band cardiac thin filaments by the I-Z-I protein network of cardiac sarcomeres.

A conventional view of the role of sarcomeric thin filaments in cardiac function is that they react with cross-bridges that translate them toward the center of the sarcomere in a reaction triggered by Ca(2+) and powered by ATP. However, thin filaments also engage in a complex network of protein-protein interactions in the Z-disc. Thus, in the modern context, understanding of what thin filaments do in the heart must take into account not only A-band regions that react with cross-bridges, but also I-Z-I regions that rarely, if ever, react with cross-bridges and dwell near and within the Z-disc. To highlight these multiplex functions of the thin filament, I discuss the hypothesis that physical and chemical reactions at the interface of the thin filaments with Z-disc proteins control the docking and activity of kinases and phosphatases that control the levels of phosphorylation of thin filament regulatory proteins. Testing this hypothesis has taken on new significance with the identification of multisite phosphorylation of thin filament proteins as a critical element in the control of cardiac contraction and relaxation reserve and in maladaptive mechanisms in heart failure. Moreover, multiple mutations in Z-disc proteins that link to prevalent cardiomyopathies are likely to alter this remote control of A-band thin filament function.

Actin Cytoskeleton↗
PubMed1995

Compliance of thin filaments in skinned fibers of rabbit skeletal muscle.

The mechanical compliance (reciprocal of stiffness) of thin filaments was estimated from the relative compliance of single, skinned muscle fibers in rigor at sarcomere lengths between 1.8 and 2.4 micron. The compliance of the fibers was calculated as the ratio of sarcomere length change to tension change during imposition of repetitive cycles of small stretches and releases. Fiber compliance decreased as the sarcomere length was decreased below 2.4 micron. The compliance of the thin filaments could be estimated from this decrement because in this range of lengths overlap between the thick and thin filaments is complete and all of the myosin heads bind to the thin filament in rigor. Thus, the compliance of the overlap region of the sarcomere is constant as length is changed and the decrease in fiber compliance is due to decrease of the nonoverlap length of the thin filaments (the I band). The compliance value obtained for the thin filaments implies that at 2.4-microns sarcomere length, the thin filaments contribute approximately 55% of the total sarcomere compliance. Considering that the sarcomeres are approximately 1.25-fold more compliant in active isometric contractions than in rigor, the thin filaments contribute approximately 44% to sarcomere compliance during isometric contraction.

Animals↗