subject:( induced contraction)

1. Hughes, William Edward. Dynamics of skeletal muscle blood flow and vasodilation with age.

Degree: PhD, Physical Rehabilitation Science, 2018, University of Iowa

► Aging is associated with attenuated blood flow and vasodilator responses during rhythmic exercise. Older adults also demonstrate attenuated blood flow and vasodilator responses following… (more)

▼ Aging is associated with attenuated blood flow and vasodilator responses during rhythmic exercise. Older adults also demonstrate attenuated blood flow and vasodilator responses following single skeletal muscle contractions (contraction-induced rapid onset vasodilation, ROV) within the forearm. These age-associated attenuations within the forearm have been demonstrated to be a result of endothelial and neural mechanisms. The objective of this research was to examine: 1) whether age-associated attenuations within the forearm are from mechanical factors; 2) whether age-associated attentions in ROV are present within the leg, as well as explore potential mechanisms for these age-associated attenuations in ROV; 3) examine whether aging is associated with a slower rate of adjustment in vasodilation (vasodilator kinetics) during rhythmic exercise preceding steady-state exercise; and 4) examine approaches to ameliorate age-related attenuations in blood flow and vasodilation within the leg across the entire exercise transient (onset to steady-state). The novel findings of this research are that 1) age-associated attenuations in ROV within the forearm are independent of mechanical factors; 2) older adults demonstrate attenuated ROV responses within the leg; 3) age-related attenuations in ROV within the leg are not explained by enhanced sympathetic adrenergic vasoconstriction; 4) older adults exhibit prolonged vasodilator kinetics preceding steady-state exercise; and 5) when examined in a cross-sectional design chronic exercise training improves ROV, vasodilator kinetics, as well as steady-state blood flow and vasodilator responses in older adults; 6) acute supplementation with dietary nitrate fails to exert any effect on blood flow and vasodilator responses during any domain of exercise. Collectively, this work establishes that aging is associated with reductions in blood flow and vasodilation across the entire exercise transient (onset to steady-state) within the leg, which is offset by chronic exercise training. Mechanistically, the current data suggests that mechanical and sympathetic factors do not explain age-related reductions in ROV in the arm and leg, respectively. Furthermore, acute supplementation of dietary nitrate does not impact leg blood flow and vasodilator responses in older adults during any domain of the exercise transient. Advisors/Committee Members: Casey, Darren P. (supervisor).

Subjects/Keywords: Blood Flow; Contraction-Induced Rapid Vasodilation; Exercise; Skeletal Muscle; Vasodilation

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APA (6^th Edition):

Hughes, W. E. (2018). Dynamics of skeletal muscle blood flow and vasodilation with age. (Doctoral Dissertation). University of Iowa. Retrieved from https://ir.uiowa.edu/etd/6142

Chicago Manual of Style (16^th Edition):

Hughes, William Edward. “Dynamics of skeletal muscle blood flow and vasodilation with age.” 2018. Doctoral Dissertation, University of Iowa. Accessed March 01, 2021. https://ir.uiowa.edu/etd/6142.

MLA Handbook (7^th Edition):

Hughes, William Edward. “Dynamics of skeletal muscle blood flow and vasodilation with age.” 2018. Web. 01 Mar 2021.

Vancouver:

Hughes WE. Dynamics of skeletal muscle blood flow and vasodilation with age. [Internet] [Doctoral dissertation]. University of Iowa; 2018. [cited 2021 Mar 01]. Available from: https://ir.uiowa.edu/etd/6142.

Council of Science Editors:

Hughes WE. Dynamics of skeletal muscle blood flow and vasodilation with age. [Doctoral Dissertation]. University of Iowa; 2018. Available from: https://ir.uiowa.edu/etd/6142

Brigham Young University

2. Deyhle, Michael Roger. The Role of T Cells in Muscle Damage Protective Adaptation.

Degree: PhD, 2018, Brigham Young University

URL: https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=8455&context=etd

► Skeletal muscle is prone to damage from a range of stimuli. The muscle repair process that ensues is complex, involving several phases and requiring… (more)

Subjects/Keywords: inflammation; exercise-induced muscle damage; repeated bout effect; flow cytometry; T lymphocyte; lengthening contraction; eccentric contraction; Life Sciences

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APA (6^th Edition):

Deyhle, M. R. (2018). The Role of T Cells in Muscle Damage Protective Adaptation. (Doctoral Dissertation). Brigham Young University. Retrieved from https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=8455&context=etd

Chicago Manual of Style (16^th Edition):

Deyhle, Michael Roger. “The Role of T Cells in Muscle Damage Protective Adaptation.” 2018. Doctoral Dissertation, Brigham Young University. Accessed March 01, 2021. https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=8455&context=etd.

MLA Handbook (7^th Edition):

Deyhle, Michael Roger. “The Role of T Cells in Muscle Damage Protective Adaptation.” 2018. Web. 01 Mar 2021.

Vancouver:

Deyhle MR. The Role of T Cells in Muscle Damage Protective Adaptation. [Internet] [Doctoral dissertation]. Brigham Young University; 2018. [cited 2021 Mar 01]. Available from: https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=8455&context=etd.

Council of Science Editors:

Deyhle MR. The Role of T Cells in Muscle Damage Protective Adaptation. [Doctoral Dissertation]. Brigham Young University; 2018. Available from: https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=8455&context=etd

University of Michigan

3. Ng, Rainer N. The occurrence of contraction-induced lesions in the sarcolemma of skeletal muscles: Insights from a micro-sized whole muscle model.

Degree: PhD, Biomedical Engineering, 2008, University of Michigan

URL: http://hdl.handle.net/2027.42/60779

► Muscles exposed to unaccustomed exercise or injurious contractile activities are likely to sustain mechanical damage to muscle fibers, a characteristic of contraction-induced injuries. The susceptibility… (more)

▼ Muscles exposed to unaccustomed exercise or injurious contractile activities are likely to sustain mechanical damage to muscle fibers, a characteristic of contraction-induced injuries. The susceptibility of muscles to contraction-induced injury increases with age, disuse or disease. Although lesions in the sarcolemma have been implicated in the injury process, the conditions that lead to the formation of such lesions, as well as the extent to which these lesions affect muscle function remain inadequately understood. To study membrane-based events reliably, we developed a micro-sized whole muscle model that was robust, but more importantly, compatible with the contemporary techniques used to study cellular function. In characterizing this muscle model in vitro, we report a level of stability and flexibility that had not been observed in previous whole muscle preparations. Utilizing this muscle model, we demonstrated that sarcolemmal lesions and overactive mechanosensitive ion channels accounted for the majority of the functional deficit observed in the diseased muscles of mdx mice, the murine model of Duchenne Muscular Dystrophy. These results provide a basis for the development of therapeutic strategies directed at stabilizing the membrane of dystrophic skeletal muscle. When wild-type muscles were subjected to an injurious protocol of lengthening contractions, the mechanical stress associated with lengthening contractions, while severe enough to cause a 30% force deficit, was found to be insufficient to elicit membrane lesions in a whole skeletal muscle. This finding diminished the role of mechanical stress as the direct cause of sarcolemmal injury and implies that contraction-induced lesions observed in wild-type muscle are likely to result from the contributions of other factors, such as reactive oxygen species and proteolytic enzyme activity. Advisors/Committee Members: Faulkner, John A. (committee member), Gafni, Ari (committee member), Herzog, Susan Brooks (committee member), Mayer, Michael (committee member).

Subjects/Keywords: Skeletal Muscles; Contraction-induced Injury; Biomedical Engineering; Engineering

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APA (6^th Edition):

Ng, R. N. (2008). The occurrence of contraction-induced lesions in the sarcolemma of skeletal muscles: Insights from a micro-sized whole muscle model. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/60779

Chicago Manual of Style (16^th Edition):

Ng, Rainer N. “The occurrence of contraction-induced lesions in the sarcolemma of skeletal muscles: Insights from a micro-sized whole muscle model.” 2008. Doctoral Dissertation, University of Michigan. Accessed March 01, 2021. http://hdl.handle.net/2027.42/60779.

MLA Handbook (7^th Edition):

Ng, Rainer N. “The occurrence of contraction-induced lesions in the sarcolemma of skeletal muscles: Insights from a micro-sized whole muscle model.” 2008. Web. 01 Mar 2021.

Vancouver:

Ng RN. The occurrence of contraction-induced lesions in the sarcolemma of skeletal muscles: Insights from a micro-sized whole muscle model. [Internet] [Doctoral dissertation]. University of Michigan; 2008. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/2027.42/60779.

Council of Science Editors:

Ng RN. The occurrence of contraction-induced lesions in the sarcolemma of skeletal muscles: Insights from a micro-sized whole muscle model. [Doctoral Dissertation]. University of Michigan; 2008. Available from: http://hdl.handle.net/2027.42/60779

University of Michigan

4. Hunter, Kam D. Contraction-induced injury: Interaction of initial length and work input.

Degree: PhD, Kinesiology, 1997, University of Michigan

URL: http://hdl.handle.net/2027.42/130263

► For single pliometric (lengthening) contractions of whole skeletal muscles initiated solely from optimal fiber length (L_f), the most important factor determining the subsequent deficit in… (more)

▼ For single pliometric (lengthening) contractions of whole skeletal muscles initiated solely from optimal fiber length (L_f), the most important factor determining the subsequent deficit in isometric force production is the work input during the stretch. The purpose of this dissertation was to clarify the association of the force deficit following pliometric contractions with specific mechanical events, using a range of initial fiber lengths to provide a more comprehensive simulation of in vivo conditions. The hypothesis was that for whole muscles when fully activated, regardless of the initial length, the force deficit following the stretch is primarily a function of the work input. Extensor digitorum longus muscles of mice were maximally activated in situ and lengthened at 2 L_f/sec from one of three initial fiber lengths (90%, 100%, or 120% of L_f) to one of three final fiber lengths (150%, 160%, or 170% of L_f). No single mechanical factor, including the work input (r² = 0.34), was sufficient to explain the differences in force deficits observed among groups. Therefore, the force deficit arises from a complex interaction of mechanical events. With the data grouped by initial fiber length, the correlation between the average work and the average force deficit was high (r² = 0.97 to 0.99). Consequently, differences in force deficits among groups were explained best on the basis of the initial fiber length and the work input during the stretch. The specific hypotheses were subsequently tested that for single permeabilized fiber segments: (i) as with whole muscles, an increased force deficit occurs following pliometric contractions initiated from longer compared with shorter fiber lengths, even when the work input is the same, and (ii) the increased force deficit at longer compared with shorter lengths is associated with an increase in the sarcomere length heterogeneity. Single permeabilized fiber segments from soleus muscles of rats were maximally activated in vitro and lengthened at 0.5 L_f/sec through one of seven protocols of varying initial and final fiber lengths. The force deficits observed following single stretches of the same relative displacements increased with increasing initial length, even though the work input was not different. For average regional sarcomere lengths, the mean and maximum increased with increasing initial length, as did the standard deviation and range. These results support the working hypothesis that following contraction-induced injury, the force deficit is a function of the sarcomere length heterogeneity, and the proportion of sarcomeres on the descending limb of the length-force curve. Advisors/Committee Members: Faulkner, John A. (advisor), Carlson, Bruce M. (advisor).

Subjects/Keywords: Contraction; Induced; Initial; Injury; Input; Interaction; Length; Work

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APA (6^th Edition):

Hunter, K. D. (1997). Contraction-induced injury: Interaction of initial length and work input. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/130263

Chicago Manual of Style (16^th Edition):

Hunter, Kam D. “Contraction-induced injury: Interaction of initial length and work input.” 1997. Doctoral Dissertation, University of Michigan. Accessed March 01, 2021. http://hdl.handle.net/2027.42/130263.

MLA Handbook (7^th Edition):

Hunter, Kam D. “Contraction-induced injury: Interaction of initial length and work input.” 1997. Web. 01 Mar 2021.

Vancouver:

Hunter KD. Contraction-induced injury: Interaction of initial length and work input. [Internet] [Doctoral dissertation]. University of Michigan; 1997. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/2027.42/130263.

Council of Science Editors:

Hunter KD. Contraction-induced injury: Interaction of initial length and work input. [Doctoral Dissertation]. University of Michigan; 1997. Available from: http://hdl.handle.net/2027.42/130263

University of Michigan

5. Rader, Erik Paul. Contraction -induced injury of weight -bearing muscles and the role of reactive oxygen species.

Degree: PhD, Biomedical engineering, 2004, University of Michigan

URL: http://hdl.handle.net/2027.42/124538

► For small, non-weight bearing muscles of old mice, severe contraction-induced injury causes a permanent 20% reduction in mass and maximum force. With aging, large, weight-bearing… (more)

▼ For small, non-weight bearing muscles of old mice, severe contraction-induced injury causes a permanent 20% reduction in mass and maximum force. With aging, large, weight-bearing muscles appear to lose mass and force more rapidly than small, non-weight-bearing muscles, yet recovery of large, weight-bearing muscles following contraction-induced injury has not been investigated. The hypothesis is tested that two months following a severe contraction-induced injury to large, weight-bearing muscles, muscles of adult mice recover, whereas those of old mice sustain permanent deficits in mass and force. For muscles of adult mice, those of male mice regained control values, while muscles of female mice sustained reductions of 9% in mass and 16% in force. For muscles of old mice, those of male mice sustained decreases of 24% in mass and 32% in force, while corresponding deficits of 14% and 40% remained for muscles of female mice. The conclusion is that a severe contraction-induced injury to large, weight-bearing muscles of old animals causes irreversible damage. Contraction-induced injury consists of an initial disruption to individual sarcomeres followed by sealing off of the focal damage and a more severe secondary injury from reactive oxygen species (ROS) released by invading inflammatory cells. The location and timing of the release of ROS relative to the sealing off process is not well documented. The hypothesis is tested that daily treatment of muscles of adult mice with a membrane permeable antioxidant, N-2-mercaptopropionyl-glycine (MPG), attenuates contraction-induced injury. Contrary to the hypothesis, no differences in force deficits were observed between muscles of antioxidant- and saline-treated mice. The results could not rule out the short residence time of MPG as a potential reason for the ineffectiveness. Therefore, the null hypothesis is tested that the continuous overexpression of genes for intracellular antioxidants has no effect on contraction-induced injury. No differences in force deficits were observed among the groups of mice. The ineffectiveness of increasing levels of intracellular antioxidants was consistent with the infiltration of inflammatory cells and release of ROS occurring predominantly at the site of the initial injury after the completion of sealing off. Advisors/Committee Members: Faulkner, John A. (advisor).

Subjects/Keywords: Contraction-induced Injury; Reactive Oxygen Species; Role; Sarcomeres; Weight-bearing Muscles

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APA (6^th Edition):

Rader, E. P. (2004). Contraction -induced injury of weight -bearing muscles and the role of reactive oxygen species. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/124538

Chicago Manual of Style (16^th Edition):

Rader, Erik Paul. “Contraction -induced injury of weight -bearing muscles and the role of reactive oxygen species.” 2004. Doctoral Dissertation, University of Michigan. Accessed March 01, 2021. http://hdl.handle.net/2027.42/124538.

MLA Handbook (7^th Edition):

Rader, Erik Paul. “Contraction -induced injury of weight -bearing muscles and the role of reactive oxygen species.” 2004. Web. 01 Mar 2021.

Vancouver:

Rader EP. Contraction -induced injury of weight -bearing muscles and the role of reactive oxygen species. [Internet] [Doctoral dissertation]. University of Michigan; 2004. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/2027.42/124538.

Council of Science Editors:

Rader EP. Contraction -induced injury of weight -bearing muscles and the role of reactive oxygen species. [Doctoral Dissertation]. University of Michigan; 2004. Available from: http://hdl.handle.net/2027.42/124538

University of Michigan

6. Lockhart, Nicole C. Mechanisms underlying the protection from contraction -induced skeletal muscle injury provided by exercising with passive stretches.

Degree: PhD, Physical therapy, 2006, University of Michigan

URL: http://hdl.handle.net/2027.42/125698

► Contraction-induced injury can occur during everyday activities when muscles are stretched while activated (lengthening contractions). Administration of passive stretches during which the muscle is lengthened… (more)

▼ Contraction-induced injury can occur during everyday activities when muscles are stretched while activated (lengthening contractions). Administration of passive stretches during which the muscle is lengthened without activation reduces the severity of injury following subsequent lengthening contractions. Contraction-induced injury is initiated by mechanical damage followed by an inflammatory response leading to a secondary injury and the degeneration of damaged muscle fibers. Conditioning with passive stretches may protect against injury by decreasing the initial mechanical damage, the secondary injury, or both. This thesis investigated potential mechanisms underlying protective adaptations induced by passive-stretch-conditioning in mice. Understanding these mechanisms is important for designing safe effective conditioning programs to reduce injury, particularly for populations susceptible to contraction-induced injury like the elderly. The best measure of the magnitude of initial mechanical damage is the deficit in force either immediately following a protocol of lengthening contractions that did not fatigue the muscle or immediately following recovery from fatigue. Shortly after lengthening contractions, the force deficits in the absence of fatigue were not different for conditioned and unconditioned muscles, supporting the conclusion that passive-stretch-conditioning does not reduce initial mechanical damage. The magnitude of the secondary injury was determined by measuring force deficits, numbers of fibers that showed morphological evidence of injury, and infiltration of muscles by inflammatory cells three days after lengthening contractions. Inhibiting nitric oxide production during passive-stretch-conditioning prevented the reduction in force deficit, number of injured fibers, and inflammation typically observed following lengthening contractions for conditioned muscles. Thus, nitric oxide produced during passive stretches appeared to have anti-inflammatory effects during subsequent lengthening contractions. Moreover, increased levels of substrate for nitric oxide production were sufficient to decrease lengthening contraction-induced force deficits, damage to fibers and inflammation, even in the absence of prior passive stretches. Passive stretches alone resulted in neutrophil infiltration of the muscle and prevention of this low level inflammatory response eliminated the protective effects of passive stretches. We conclude that passive-stretch-conditioning reduces injury following subsequent lengthening contractions not by decreasing initial mechanical damage, but through a reduction in the secondary injury, specifically by blunting inflammation. Advisors/Committee Members: Herzog, Susan Brooks (advisor).

Subjects/Keywords: Contraction-induced; Exercising; Mechanisms; Muscle Injury; Passive Stretches; Protection; Provided; Skeletal Muscle; Underlying

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APA (6^th Edition):

Lockhart, N. C. (2006). Mechanisms underlying the protection from contraction -induced skeletal muscle injury provided by exercising with passive stretches. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/125698

Chicago Manual of Style (16^th Edition):

Lockhart, Nicole C. “Mechanisms underlying the protection from contraction -induced skeletal muscle injury provided by exercising with passive stretches.” 2006. Doctoral Dissertation, University of Michigan. Accessed March 01, 2021. http://hdl.handle.net/2027.42/125698.

MLA Handbook (7^th Edition):

Lockhart, Nicole C. “Mechanisms underlying the protection from contraction -induced skeletal muscle injury provided by exercising with passive stretches.” 2006. Web. 01 Mar 2021.

Vancouver:

Lockhart NC. Mechanisms underlying the protection from contraction -induced skeletal muscle injury provided by exercising with passive stretches. [Internet] [Doctoral dissertation]. University of Michigan; 2006. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/2027.42/125698.

Council of Science Editors:

Lockhart NC. Mechanisms underlying the protection from contraction -induced skeletal muscle injury provided by exercising with passive stretches. [Doctoral Dissertation]. University of Michigan; 2006. Available from: http://hdl.handle.net/2027.42/125698

7. 王, 志丹. Caffeine inhibits smooth muscle actin-myosin interaction : カフェインは平滑筋ミオシンアクチン相互作用を抑制する.

Degree: 修士（健康科学）, 2017, Tokyo Metropolitan University / 首都大学東京

URL: http://hdl.handle.net/10748/00009635

►

Caffeine is known to have inhibitory effects on Ca^<2+>-induced contraction in smooth muscle, and possible mechanisms may contribute the inhibitory effects. Recently, it was found… (more)

▼

Caffeine is known to have inhibitory effects on Ca^<2+>-induced contraction in smooth muscle, and possible mechanisms may contribute the inhibitory effects. Recently, it was found a caffeine effect on direct inhibition of myosin-actin interaction in smooth muscle. To clarify whether direct inhibition of myosin-actin interaction of caffeine to be dependent on the regulation of myosin light chain phosphorylation, in the present study, the author examined caffeine effects on skinned (cell membrane permeabilized) smooth muscle contraction. At 10 mM, caffeine significantly suppressed Ca^<2+> induced contraction, which was dependent on myosin light chain phosphorylation. On the other hand, caffeine did not affect 15.5 mM Mg^<2+> induced contraction, which was independent of myosin light chain phosphorylation. The present results suggest that caffeine inhibits actin-myosin interaction of smooth muscle through either inhibition of myosin light chain kinase activity or acceleration of myosin phosphatase activity.

カフェインには平滑筋にCaイオンの抑制があることが知られている。様々な機構がこの抑制に関与している。最近、カフェインは平滑筋のミオシンアクチン相互作用を直接的に抑制することが明らかになった。本研究では、細胞膜を破壊したスキンド盲腸紐標本を用いて、カフェインの平滑筋アクチン・ミオシン相互作用の抑制が、ミオシン軽鎖リン酸化の抑制によるものなのかを検討した。10mMのカェインはミオシン軽鎖リン酸化に依存するCaイオン活性化収縮張力を抑制した。一方、カフェインはミオシン軽鎖リン酸化に依存しない15.5mM Mgイオンによる収縮張力を抑制しない。以上から、カフェインはミオシン軽鎖リン酸化酵素の活性阻害、もしくはミオシンボスファターゼの活性を促進することでミオシン軽鎖リン酸化レベルを低下させることで、平滑筋ミオシンアクチン相互作用を抑制し、平滑筋収縮を抑制することが示唆された。

首都大学東京, 2017-03-25, 修士（健康科学）

Subjects/Keywords: caffeine; Ca^<; 2+>; -induced contraction; myosin-actin interaction; myosin light chain phosphorylation; カフェイン; Ca^<; 2+>; 活性化収縮; ミオシン-アクチン相互作用; ミオシン軽鎖リン酸化

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APA (6^th Edition):

王, �. (2017). Caffeine inhibits smooth muscle actin-myosin interaction : カフェインは平滑筋ミオシンアクチン相互作用を抑制する. (Thesis). Tokyo Metropolitan University / 首都大学東京. Retrieved from http://hdl.handle.net/10748/00009635

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

王, 志丹. “Caffeine inhibits smooth muscle actin-myosin interaction : カフェインは平滑筋ミオシンアクチン相互作用を抑制する.” 2017. Thesis, Tokyo Metropolitan University / 首都大学東京. Accessed March 01, 2021. http://hdl.handle.net/10748/00009635.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

王, 志丹. “Caffeine inhibits smooth muscle actin-myosin interaction : カフェインは平滑筋ミオシンアクチン相互作用を抑制する.” 2017. Web. 01 Mar 2021.

Vancouver:

王 �. Caffeine inhibits smooth muscle actin-myosin interaction : カフェインは平滑筋ミオシンアクチン相互作用を抑制する. [Internet] [Thesis]. Tokyo Metropolitan University / 首都大学東京; 2017. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/10748/00009635.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

王 �. Caffeine inhibits smooth muscle actin-myosin interaction : カフェインは平滑筋ミオシンアクチン相互作用を抑制する. [Thesis]. Tokyo Metropolitan University / 首都大学東京; 2017. Available from: http://hdl.handle.net/10748/00009635

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Michigan

8. Panchangam, Appaji. Sarcomere Dynamics During Contraction-Induced Injury to Permeabilized Single Muscle Fibers.

Degree: PhD, Biomedical Engineering, 2008, University of Michigan

URL: http://hdl.handle.net/2027.42/58375

► A contraction-induced injury results when an activated skeletal muscle or a single fiber is stretched in a ‘lengthening contraction’. This type of injury to muscle… (more)

▼ A contraction-induced injury results when an activated skeletal muscle or a single fiber is stretched in a ‘lengthening contraction’. This type of injury to muscle fibers is a leading cause of the loss of mobility that is associated with old age. Manifestations of the injury revealed by electron microscopy show focally disrupted single sarcomeres, or small groups of sarcomeres, that are surrounded by intact sarcomeres. The purpose of this dissertation was to study the dynamic behavior of sarcomeres during lengthening contractions of single muscle fibers. The working hypothesis was that contraction-induced injury occurs during a lengthening contraction when sarcomeres undergo elongation at varying rates and those lengthened at the highest rates reach longer lengths and are damaged. To test this hypothesis, a laser scanning system was developed that recorded rapidly (500 s−1) the lengths of sarcomeres contained in each of 20 contiguous regions along ~1 mm segments of a fiber. The fiber segments were obtained from soleus muscles of adult male rats and the membranes of the fibers were permeabilized chemically. The experiments performed with the laser scanning apparatus, indicated that: (i) during a lengthening contraction, the regions of fibers that contain the longer sarcomeres at the onset of the lengthening elongate more compared with the regions that contain shorter sarcomeres; (ii) lengthening contractions increased the variability in the lengths of sarcomeres in relaxed fibers; and (iii) during a lengthening contraction, within any given fiber region, the rate of elongation of sarcomeres was stable, but different regions stretched at different rates as the contraction proceeded. The present findings support the hypothesis that, within single fibers, non-uniformities develop in the lengths of sarcomeres that are increased by a lengthening contraction. The finding that all fiber regions elongate at stable rates during lengthening contractions contradicts a previous hypothesis that during lengthening contractions, the longest sarcomeres undergo rapid and sudden elongation to extreme lengths. The conclusion is that during lengthening contractions, the longer sarcomeres in series with shorter sarcomeres undergo elongation at higher velocities and upon return to original length, structural elements within some of these longer sarcomeres are functionally compromised. Advisors/Committee Members: Faulkner, John A. (committee member), Claflin, Dennis R. (committee member), Noll, Douglas C. (committee member), Palmer, Mark Lawson (committee member), Steel, Duncan G. (committee member).

Subjects/Keywords: Sarcomere Dynamics; Sarcomere Non-uniformity; Sarcomere Heterogeneity; Contraction-induced Injury; Laser Scanning; Sarcomere Length; Engineering; Health Sciences

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APA (6^th Edition):

Panchangam, A. (2008). Sarcomere Dynamics During Contraction-Induced Injury to Permeabilized Single Muscle Fibers. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/58375

Chicago Manual of Style (16^th Edition):

Panchangam, Appaji. “Sarcomere Dynamics During Contraction-Induced Injury to Permeabilized Single Muscle Fibers.” 2008. Doctoral Dissertation, University of Michigan. Accessed March 01, 2021. http://hdl.handle.net/2027.42/58375.

MLA Handbook (7^th Edition):

Panchangam, Appaji. “Sarcomere Dynamics During Contraction-Induced Injury to Permeabilized Single Muscle Fibers.” 2008. Web. 01 Mar 2021.

Vancouver:

Panchangam A. Sarcomere Dynamics During Contraction-Induced Injury to Permeabilized Single Muscle Fibers. [Internet] [Doctoral dissertation]. University of Michigan; 2008. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/2027.42/58375.

Council of Science Editors:

Panchangam A. Sarcomere Dynamics During Contraction-Induced Injury to Permeabilized Single Muscle Fibers. [Doctoral Dissertation]. University of Michigan; 2008. Available from: http://hdl.handle.net/2027.42/58375

University of Michigan

9. Consolino, Christina Marie. The role of the dystrophin -glycoprotein complex in the structure, function, and susceptibility to contraction -induced injury of limb muscles in dystrophic mice.

Degree: PhD, Kinesiology, 2003, University of Michigan

URL: http://hdl.handle.net/2027.42/123367

► The dystrophin glycoprotein complex (DGC) physically links cytoskeletal actin to the extracellular matrix (ECM) of skeletal muscle fibers, and mutations in the genes encoding many… (more)

▼ The dystrophin glycoprotein complex (DGC) physically links cytoskeletal actin to the extracellular matrix (ECM) of skeletal muscle fibers, and mutations in the genes encoding many members of the DGC result in muscular dystrophy. Primary deficiencies of two proteins, dystrophin and alpha-sarcoglycan, destabilize the entire DGC in mdx and Sgca-null mice, respectively. The purpose was to examine the structure, function and susceptibility to contraction-induced injury of limb muscles of Sgca-null and mdx mice to elucidate the function of the DGC. The working hypothesis was that the DGC shunts contractile forces laterally from the myofibrils through the plasma membrane to the ECM, and deficiencies in the DGC result in a mechanically compromised cytoskeleton, increasing sarcomere heterogeneity and susceptibility to damage. Contractile and morphological properties of extensor digitorum longus (EDL) and soleus muscles of Sgca-null and wild type mice were compared, and the responses of muscles of Sgca-null and mdx mice to contraction-induced injury induced by single stretches were investigated. Compared with muscles of wild type mice, muscles of Sgca-null mice maintained 40% to 100% greater masses throughout the life span, resulting primarily from the accumulation of noncontractile material. Increases in fiber number provided some compensation for the presence of degenerating fibers in muscles of Sgca-null mice as evidenced by absolute forces and powers at or above control values. Similar forces and powers of alpha-sarcoglycan deficient and wild type muscles coupled with large masses of muscles of Sgca-null mice resulted in low specific forces and normalized powers. An exception was that soleus muscles of male Sgca-null mice employed additional, but as yet unknown, adaptations to compensate for the alpha-sarcoglycan deficiency resulting in control levels of specific force and normalized power. Compared with respective control muscles, greater force deficits were observed following single stretches of maximally activated EDL muscles of mdx mice and EDL and soleus muscles of Sgca-null mice with no indications of membrane damage. The findings are consistent with a role for the DGC in the stabilization of the alignment of sarcomeres, in addition to the previously accepted role in conferring structural support to the muscle fiber membrane. Advisors/Committee Members: Herzog, Susan V. Brooks (advisor), Westfall, Margaret V. (advisor).

Subjects/Keywords: Complex; Contraction-induced Injury; Dystrophic; Dystrophin-glycoprotein; Function; Limb Muscles; Mice; Muscular Dystrophy; Role; Structure; Susceptibility

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APA (6^th Edition):

Consolino, C. M. (2003). The role of the dystrophin -glycoprotein complex in the structure, function, and susceptibility to contraction -induced injury of limb muscles in dystrophic mice. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/123367

Chicago Manual of Style (16^th Edition):

Consolino, Christina Marie. “The role of the dystrophin -glycoprotein complex in the structure, function, and susceptibility to contraction -induced injury of limb muscles in dystrophic mice.” 2003. Doctoral Dissertation, University of Michigan. Accessed March 01, 2021. http://hdl.handle.net/2027.42/123367.

MLA Handbook (7^th Edition):

Consolino, Christina Marie. “The role of the dystrophin -glycoprotein complex in the structure, function, and susceptibility to contraction -induced injury of limb muscles in dystrophic mice.” 2003. Web. 01 Mar 2021.

Vancouver:

Consolino CM. The role of the dystrophin -glycoprotein complex in the structure, function, and susceptibility to contraction -induced injury of limb muscles in dystrophic mice. [Internet] [Doctoral dissertation]. University of Michigan; 2003. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/2027.42/123367.

Council of Science Editors:

Consolino CM. The role of the dystrophin -glycoprotein complex in the structure, function, and susceptibility to contraction -induced injury of limb muscles in dystrophic mice. [Doctoral Dissertation]. University of Michigan; 2003. Available from: http://hdl.handle.net/2027.42/123367

10. PORKODI PANNEERSELVAM. MITOCHONDRIA LOCALIZED TLR ADAPTOR SARM IS PROAPOPTOTIC DURING T-CELL IMMUNE RESPONSE.

Degree: 2012, National University of Singapore

URL: http://scholarbank.nus.edu.sg/handle/10635/35245

Subjects/Keywords: Influenza infection mouse model; proapoptotic SARM; T-cell contraction; neglect- and activation-induced T-cell death; NK/T cell lymphoma

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APA (6^th Edition):

PANNEERSELVAM, P. (2012). MITOCHONDRIA LOCALIZED TLR ADAPTOR SARM IS PROAPOPTOTIC DURING T-CELL IMMUNE RESPONSE. (Thesis). National University of Singapore. Retrieved from http://scholarbank.nus.edu.sg/handle/10635/35245

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

PANNEERSELVAM, PORKODI. “MITOCHONDRIA LOCALIZED TLR ADAPTOR SARM IS PROAPOPTOTIC DURING T-CELL IMMUNE RESPONSE.” 2012. Thesis, National University of Singapore. Accessed March 01, 2021. http://scholarbank.nus.edu.sg/handle/10635/35245.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

PANNEERSELVAM, PORKODI. “MITOCHONDRIA LOCALIZED TLR ADAPTOR SARM IS PROAPOPTOTIC DURING T-CELL IMMUNE RESPONSE.” 2012. Web. 01 Mar 2021.

Vancouver:

PANNEERSELVAM P. MITOCHONDRIA LOCALIZED TLR ADAPTOR SARM IS PROAPOPTOTIC DURING T-CELL IMMUNE RESPONSE. [Internet] [Thesis]. National University of Singapore; 2012. [cited 2021 Mar 01]. Available from: http://scholarbank.nus.edu.sg/handle/10635/35245.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

PANNEERSELVAM P. MITOCHONDRIA LOCALIZED TLR ADAPTOR SARM IS PROAPOPTOTIC DURING T-CELL IMMUNE RESPONSE. [Thesis]. National University of Singapore; 2012. Available from: http://scholarbank.nus.edu.sg/handle/10635/35245

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

11. Krishna, Abhilash. Multiphysics model of a cardiac myocyte: A voltage-clamp study.

Degree: PhD, Engineering, 2013, Rice University

URL: http://hdl.handle.net/1911/71664

► We develop a composite multiphysics model of excitation-contraction coupling for a rat ventricular myocyte under voltage clamp (VC) conditions to: (1) probe mechanisms underlying the… (more)

▼ We develop a composite multiphysics model of excitation-contraction coupling for a rat ventricular myocyte under voltage clamp (VC) conditions to: (1) probe mechanisms underlying the response to Ca2+-perturbation; (2) investigate the factors influencing its electromechanical response; and (3) examine its rate-dependent behavior (particularly the force-frequency response (FFR)). Motivation for the study was to pinpoint key control variables influencing calcium-induced calcium-release (CICR) and examine its role in the context of a physiological control system regulating cytosolic Ca2+ concentration and hence the cardiac contractile response. Our cell model consists of an electrical-equivalent model for the cell membrane and a fluid-compartment model describing the flux of ionic species between the extracellular and several intracellular compartments. The model incorporates frequency-dependent calmodulin (CaM) mediated spatially heterogenous interaction of calcineurin (CaN) and Ca2+/calmodulin-dependent protein kinase-II (CaMKII) with their principal targets and accounts for rate-dependent, cyclic adenosine monophosphate (cAMP)-mediated up-regulation. We also incorporate a biophysical model for cardiac contractile mechanics to study the factors influencing force response. The model reproduces measured VC data published by several laboratories, and generates graded Ca2+-release with high Ca2+ gain by achieving negative feedback control and Ca2+-homeostasis. We examine the dependence of cellular contractile response on: (1) the amount of activator Ca2+ available; (2) the type of mechanical load applied; (3) temperature (22 to 38ºC); and (4) myofilament Ca2+ sensitivity. We demonstrate contraction-relaxation coupling over a wide range of physiological perturbations. Our model reproduces positive peak FFR observed in rat ventricular myocytes and provides quantitative insight into the underlying rate-dependence of CICR. The role of Ca2+ regulating mechanisms are examined in handling induced Ca2+-perturbations using a rigorous cellular Ca2+ balance. Extensive testing of the composite model elucidates the importance of various direct and indirect modulatory influences on the cellular twitch-response with wide agreement with measured data on all accounts. We identify cAMP-mediated stimulation, and rate-dependent CaMKII-mediated up-regulation of Ca2+-trigger current (ICaL) as the key mechanisms underlying the aforementioned positive FFR. Our model provides biophysically-based explanations of phenomena associated with CICR and provides mechanistic insights into whole-cell responses to a wide variety of testing approaches used in studies of cardiac myofilament contractility. Advisors/Committee Members: Clark, John W., Jr. (advisor), Cavallaro, Joseph R. (committee member), Dick, Andrew J. (committee member).

Subjects/Keywords: Multiphysics model; Excitation-contraction coupling; Rats; Ventricular myocyte; Voltage clamp; Electromechanics; FFR; Force-frequency response; CICR; Calcium-induced calcium-release; Myofilament contraction

…Secondary [Ca2+ ]myo Transients Induced by “Tail Currents” . 96 3.3.16 Cytosolic… …Contraction on the [Ca2+ ]myo Transient . . . . . . . 122 4.3.3 Regulation of Isometric… …Secondary [Ca2+ ]myo transients induced by “tail currents” . . . . . . 99 3.16… …contraction . . . . . . . . . . . . . . . . . . . . . . . . 115 4.2 Unloaded contraction… …117 4.3 Isometric contraction . . . . . . . . . . . . . . . . . . . . . . . . . . . 119…

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Krishna, A. (2013). Multiphysics model of a cardiac myocyte: A voltage-clamp study. (Doctoral Dissertation). Rice University. Retrieved from http://hdl.handle.net/1911/71664

Chicago Manual of Style (16^th Edition):

Krishna, Abhilash. “Multiphysics model of a cardiac myocyte: A voltage-clamp study.” 2013. Doctoral Dissertation, Rice University. Accessed March 01, 2021. http://hdl.handle.net/1911/71664.

MLA Handbook (7^th Edition):

Krishna, Abhilash. “Multiphysics model of a cardiac myocyte: A voltage-clamp study.” 2013. Web. 01 Mar 2021.

Vancouver:

Krishna A. Multiphysics model of a cardiac myocyte: A voltage-clamp study. [Internet] [Doctoral dissertation]. Rice University; 2013. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/1911/71664.

Council of Science Editors:

Krishna A. Multiphysics model of a cardiac myocyte: A voltage-clamp study. [Doctoral Dissertation]. Rice University; 2013. Available from: http://hdl.handle.net/1911/71664

Leiden University

12. Meer, van, B.J. Quantifying functional phenotypes in human pluripotent stem cell derived cardiomyocytes for disease modelling and drug discovery.

Degree: 2020, Leiden University

URL: http://hdl.handle.net/1887/138008

► Studying diseases or effects of new drugs on the human body is challenging, not least because of the lack of proper testing models that recapitulate… (more)

Subjects/Keywords: Human induced pluripotent stem cell (hiPSC); Human induced pluripotent stem cell-derived cardiomyocyte (hiPSC-CM); Cardiomyocytes; Cardiac contractility; Organ-on-Chip (OoC); Microphysiological systems (MPS); Drug testing; Disease modelling; Contraction-excitation coupling; Heart; Human induced pluripotent stem cell (hiPSC); Human induced pluripotent stem cell-derived cardiomyocyte (hiPSC-CM); Cardiomyocytes; Cardiac contractility; Organ-on-Chip (OoC); Microphysiological systems (MPS); Drug testing; Disease modelling; Contraction-excitation coupling; Heart

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Meer, van, B. J. (2020). Quantifying functional phenotypes in human pluripotent stem cell derived cardiomyocytes for disease modelling and drug discovery. (Doctoral Dissertation). Leiden University. Retrieved from http://hdl.handle.net/1887/138008

Chicago Manual of Style (16^th Edition):

Meer, van, B J. “Quantifying functional phenotypes in human pluripotent stem cell derived cardiomyocytes for disease modelling and drug discovery.” 2020. Doctoral Dissertation, Leiden University. Accessed March 01, 2021. http://hdl.handle.net/1887/138008.

MLA Handbook (7^th Edition):

Meer, van, B J. “Quantifying functional phenotypes in human pluripotent stem cell derived cardiomyocytes for disease modelling and drug discovery.” 2020. Web. 01 Mar 2021.

Vancouver:

Meer, van BJ. Quantifying functional phenotypes in human pluripotent stem cell derived cardiomyocytes for disease modelling and drug discovery. [Internet] [Doctoral dissertation]. Leiden University; 2020. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/1887/138008.

Council of Science Editors:

Meer, van BJ. Quantifying functional phenotypes in human pluripotent stem cell derived cardiomyocytes for disease modelling and drug discovery. [Doctoral Dissertation]. Leiden University; 2020. Available from: http://hdl.handle.net/1887/138008

Colorado State University

13. Simpson, Carrie Beth. Acute ascorbic acid administration improves exercise hyperemia during rhythmic but not single contractions in aging humans.

Degree: MS(M.S.), Health and Exercise Science, 2009, Colorado State University

URL: http://hdl.handle.net/10217/23287

► Age-related increases in oxidative stress are known to impair endothelium dependent vasodilation in older healthy humans. As a result, many researchers have speculated that endothelial… (more)

▼ Age-related increases in oxidative stress are known to impair endothelium dependent vasodilation in older healthy humans. As a result, many researchers have speculated that endothelial dysfunction contributes to impaired muscle blood flow and vascular control during exercise. Further, elevations in oxidative stress and subsequent endothelial dysfunction could possibly explain our recent observations of impaired contraction-induced rapid vasodilation in older adults. Therefore, we directly tested the hypothesis that acute ascorbic acid administration would augment (1) rapid vasodilation in response to single muscle contractions as well as (2) the hyperemic response to sustained rhythmic contractions in older healthy humans, and that this would be due to improved endothelium-dependent vasodilation. In 14 young (22±1 yrs) and 14 healthy older men and women (65±2 yrs), we measured forearm blood flow (FBF; Doppler ultrasound) and calculated vascular conductance (FVC) responses to single, 1 second dynamic contractions at 10, 20, and 40% maximum voluntary contraction (MVC) before and after intra-arterial administration of ascorbic acid (AA). We also measured these variables during rhythmic handgrip exercise at 10% maximum voluntary contraction. After 5 minutes of steady-state exercise with saline, ascorbic acid (AA) was infused via brachial artery catheter for 10 minutes during continued exercise. For single contractions, prior to AA peak vasodilator responses to all contraction intensities were impaired ~35-50% in older adults (P<0.05), as were the immediate (1st cardiac cycle post contraction) vasodilator responses at 20 and 40% MVC (~50%; P<0.05). In contrast to our hypothesis, AA did not influence contraction-induced rapid vasodilation in either group (all NS). Regarding rhythmic handgrip exercise, FBF (~28%) and FVC (~31%) were lower in older vs young adults (P=0.06 and P<0.05) prior to AA. In young adults, AA administration did not significantly influence FBF and FVC, whereas FBF and FVC increased 30±4% in older adults at end exercise (P<0.05). AA did not influence vasodilator responses to sodium nitroprusside in either group, but significantly improved vasodilation to acetylcholine in older adults only (P<0.05). We conclude that endothelial dysfunction is not the primary mechanism underlying impaired contraction-induced rapid vasodilation with human aging; however acute AA administration increases muscle blood flow during dynamic exercise in older adults, which is likely due to an improvement in endothelium dependent vasodilation. Advisors/Committee Members: Dinenno, Frank A. (advisor), Earley, Scott (committee member), Bell, Christopher (committee member).

Subjects/Keywords: acute AA administration; acute ascorbic acid administration; oxidative stress; endothelial dysfunction; contraction-induced rapid vasodilation; older adults; aging; exercise hyperaemia; Vitamin C – Physiological effect; Older people – Exercise – Physiological aspects; Oxidative stress; Vascular endothelium; Blood-vessels – Dilatation

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Simpson, C. B. (2009). Acute ascorbic acid administration improves exercise hyperemia during rhythmic but not single contractions in aging humans. (Masters Thesis). Colorado State University. Retrieved from http://hdl.handle.net/10217/23287

Chicago Manual of Style (16^th Edition):

Simpson, Carrie Beth. “Acute ascorbic acid administration improves exercise hyperemia during rhythmic but not single contractions in aging humans.” 2009. Masters Thesis, Colorado State University. Accessed March 01, 2021. http://hdl.handle.net/10217/23287.

MLA Handbook (7^th Edition):

Simpson, Carrie Beth. “Acute ascorbic acid administration improves exercise hyperemia during rhythmic but not single contractions in aging humans.” 2009. Web. 01 Mar 2021.

Vancouver:

Simpson CB. Acute ascorbic acid administration improves exercise hyperemia during rhythmic but not single contractions in aging humans. [Internet] [Masters thesis]. Colorado State University; 2009. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/10217/23287.

Council of Science Editors:

Simpson CB. Acute ascorbic acid administration improves exercise hyperemia during rhythmic but not single contractions in aging humans. [Masters Thesis]. Colorado State University; 2009. Available from: http://hdl.handle.net/10217/23287

Leiden University

14. Halaidych, O.V. Towards functional analysis of cerebrovascular cell types derived from human induced pluripotent stem cells.

Degree: 2019, Leiden University

URL: http://hdl.handle.net/1887/80758

► The work presented in this thesis provides novel contributions to advanced quantitative functional assessment of vascular endothelial and smooth muscle cells differentiated from hiPSCs. The automated assays… (more)

Subjects/Keywords: Human Induced Pluripotent Stem Cells; hiPSC-derived endothelial cells; hiPSC-derived smooth muscle cells; endothelial cell barrier function; impedance spectroscopy; junctional integrity; inflammatory responses; Ca2+ release; cell contraction; automated image analysis; Human Induced Pluripotent Stem Cells; hiPSC-derived endothelial cells; hiPSC-derived smooth muscle cells; endothelial cell barrier function; impedance spectroscopy; junctional integrity; inflammatory responses; Ca2+ release; cell contraction; automated image analysis

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Halaidych, O. V. (2019). Towards functional analysis of cerebrovascular cell types derived from human induced pluripotent stem cells. (Doctoral Dissertation). Leiden University. Retrieved from http://hdl.handle.net/1887/80758

Chicago Manual of Style (16^th Edition):

Halaidych, O V. “Towards functional analysis of cerebrovascular cell types derived from human induced pluripotent stem cells.” 2019. Doctoral Dissertation, Leiden University. Accessed March 01, 2021. http://hdl.handle.net/1887/80758.

MLA Handbook (7^th Edition):

Halaidych, O V. “Towards functional analysis of cerebrovascular cell types derived from human induced pluripotent stem cells.” 2019. Web. 01 Mar 2021.

Vancouver:

Halaidych OV. Towards functional analysis of cerebrovascular cell types derived from human induced pluripotent stem cells. [Internet] [Doctoral dissertation]. Leiden University; 2019. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/1887/80758.

Council of Science Editors:

Halaidych OV. Towards functional analysis of cerebrovascular cell types derived from human induced pluripotent stem cells. [Doctoral Dissertation]. Leiden University; 2019. Available from: http://hdl.handle.net/1887/80758

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