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Lower Limb Muscles
Published in Eve K. Boyle, Vondel S. E. Mahon, Rui Diogo, Handbook of Muscle Variations and Anomalies in Humans, 2022
Eve K. Boyle, Vondel S. E. Mahon, Rui Diogo, Malynda Williams
Pettersen (1979) found that quadratus plantae was rudimentary in both feet of a boy with trisomy 13q. In both feet, the lateral head was absent. In the left foot, the medial head was diminutive and originated from the posteromedial aspect of the calcaneus near the insertion of the calcaneal tendon. The muscle did not have fleshy fibers as it crossed the longitudinal arch of the foot. It had a “weblike” attachment onto the deep surface of flexor digitorum brevis, into the part of the flexor hallucis longus tendon that unites with flexor digitorum longus, and into the deep plantar fascia and ligaments of the foot. In the right foot, the medial head had a similar origin and was also diminutive but sent fleshy fibers across the foot that ended with a tendinous attachment into flexor digitorum longus. Hootnick et al. (1987) describe an individual that had a right limb with congenital tibial aplasia, talocalcaneal synchondrosis, and an adducted foot with five toes. In this limb, quadratus plantae originated from the calcaneus and inserted into the common flexor tendon sheet in the foot.
Lower limb
Published in David Heylings, Stephen Carmichael, Samuel Leinster, Janak Saada, Bari M. Logan, Ralph T. Hutchings, McMinn’s Concise Human Anatomy, 2017
David Heylings, Stephen Carmichael, Samuel Leinster, Janak Saada, Bari M. Logan, Ralph T. Hutchings
Muscles of the sole - like the palm of the hand, the sole has separate muscles for the great and little toes, as well as others with multiple tendons. Of the larger and more important muscles, flexor digitorum brevis is the central superficial muscle of the sole, immediately deep to the plantar aponeurosis (it corresponds to flexor digitorum superficialis in the hand), with tendons to the middle phalanges of the four lateral toes splitting to allow the tendons of flexor digitorum longus to pass through to the distal phalanges (Fig.8.18). Quadratus plantae, sometimes called flexor accessorius, is deep to brevis, attaching to flexor digitorum longus (just before that muscleFlexor hallucis longus splits into its four tendons) and supposedly counteracts the slightly oblique pull of longus. The lumbrical and interosseous muscles have similar attachments to those of the hand, and are important in keeping the toes straight (i.e. flexing the metatarsophalangeal joints and extending the interphalangeal joints).
Biomechanical modelling and simulation of foot and ankle
Published in Youlian Hong, Roger Bartlett, Routledge Handbook of Biomechanics and Human Movement Science, 2008
A relatively detailed 2D foot model in terms of soft tissue modelling was developed by Wu41 using CT and MR images. The second and fifth rays were chosen to model the medial and lateral longitudinal foot arches, which included the cortical and trabecular bones, cartilages, fat pad, major plantar ligamentous structures and 11 associated muscles and tendons. Except the intrinsic muscle tissue and the cartilaginous structures between the toes were defined as hyperelastic, the rest of the modelled structures were assumed to be linearly elastic. Three different stiffness of intrinsic muscle tissue, plantar fasciotomy, and major plantar ligament injuries were analyzed in balanced standing. Fasciotomy increased the peak stresses in the bones, and shifted the maximum stresses to the second metatarsal and the long plantar ligament attachment area for more than 100 per cent. About 65 per cent increases in maximum strain of the long plantar ligament was predicted. With simulated plantar ligament injuries, the plantar fascia and flexor tendon sustained increased peak stresses of about 40 per cent and 30 per cent, respectively while the bony structures sustained similar stress increases as with fasciotomy. The predicted intrinsic muscle stresses in the intact foot was minimal. Increasing the passive tensions of intrinsic muscles in the injured foot decreased the stress levels to close to the intact foot but resulted in about 20 times increase in peak muscle stresses of the flexor digitorum brevis and abductor digiti minimi. It was speculated that fasciotomy may lead to metatarsal stress fractures, whereas, strengthening intrinsic muscle passive tensions may reduce the risk of developing plantar fasciitis and related forefoot pain and metatarsal fracture.
Impaired neuromuscular function by conjoint actions of organophosphorus insecticide metabolites omethoate and cyclohexanol with implications for treatment of respiratory failure
Published in Clinical Toxicology, 2021
Kosala N. Dissanayake, Robert Chang-Chih Chou, Adrian Thompson, Filip Margetiny, Charlotte Davie, Scott McKinnon, Vishwendra Patel, Lester Sultatos, Joseph J. McArdle, Richard E. Clutton, Michael Eddleston, Richard R. Ribchester
For isolation of nerve-muscle preparations, mice were sacrificed in accordance with UK Home Office Schedule 1, by anaesthetic overdose followed by cervical dislocation. Nerve-muscle preparations of flexor digitorum brevis (FDB), hemidiaphragm, or triangularis sterni (TS) [34,37] were promptly dissected and maintained in mammalian physiological saline (MPS) with the following composition (mM): Na+ (158); K+ (5); Ca2+ (2); Mg2+ (1); Cl− (169); glucose (5); HEPES (5); pH 7.2–7.4. Solutions were bubbled with air for at least 20 min. Most experiments were conducted at room temperature (19–25 °C). Dimethoate, omethoate, cyclohexanone, cyclohexanol or xylene (all Sigma-Aldrich) were added directly from aqueous stock solutions to bathing solutions to give the concentrations required. Aliquots (10–100 µl) were either pipetted directly and thoroughly mixed into MPS in the recording chamber to the required concentration, or solutions containing the required final concentration in 50 ml volumes were rapidly exchanged with the solution in the recording chamber (volume approximately 10 ml) using coupled back-to-back 20–50 ml syringes connected to ports at opposite ends of the chamber. Baffles built into the chamber facilitated laminar flow and complete solution exchange occurred within 5–20 s.
Cooling down the use of cryotherapy for post-exercise skeletal muscle recovery*
Published in Temperature, 2018
Within the same study, the potential intramuscular mechanisms underlying the temperature-dependent recovery of muscle function were investigated in intact single muscle fibres from mouse flexor digitorum brevis. A major advantage of the intact single fibre technique employed in our study is that Ca2+ is a known major regulator of skeletal muscle force generation and this preparation allows us to determine how fatigue-induced changes in intracellular Ca2+ handling affect contractile force [3]. In our study, all muscle fibres were fatigued with repeated submaximal contractions (31°C), but thereafter fibres were separated into four different recovery temperatures where they were cooled (16°C, 26°C), not treated (31°C) or heated above the in-vivo physiological temperature of the mouse flexor digitorum brevis muscle (36°C). Recovery of contractile function was assessed by stimulating muscle fibres every 30 min during the 2 h recovery period. The results from these experiments revealed that cooling skeletal muscle fibres depressed the recovery of sarcoplasmic reticulum Ca2+ release and submaximal force, whereas heating improved recovery. Some fibres underwent a fatigue test involving repeated contractions following the recovery period, and comparable to the result in the human studies, we were able to show that fatigue resistance was impaired in fibres that underwent cooling versus heating in the recovery period.
Restoration of dystrophin expression and correction of Duchenne muscular dystrophy by genome editing
Published in Expert Opinion on Biological Therapy, 2021
Tejal Aslesh, Esra Erkut, Toshifumi Yokota
There have also been advancements in the mouse model being deployed in the studies. For example, studies have moved from the classical models that originated in the eighties: mdx mouse [40] and mdx4cv mouse with a nonsense mutation in exon 53 [64] (which has at least 10 times fewer revertant fibers than the mdx model) to the humanized ΔEx52 mouse, which carries the human DMD gene sequence with a deletion mutation of exon 52 [65]. t’ Hoen et al. generated transgenic mice with stable integration of the full-length human DMD transgene (hDMD) on chromosome 5 [66]. They observed similar tissue-specific expression patterns of various DMD isoforms in the humanized mouse model. Following the cross between the hDMD mice with mdx utrophin knockout mdx mice called dko mice, the transgene was capable of rescuing the lethal phenotype of dko mice. Young et al. created another humanized mouse model, since the previous humanized mouse model expressed the WT DMD transcript and does not represent the dystrophic phenotype [63]. They used the CRISPR/Cas9 system to create an out-of-frame mutation by deleting exon 45 of the human DMD gene in mouse zygotes (hDMD ΔEx45 mice) via NHEJ [63]. They crossed these hDMD ΔEx45 mice to both the mdx (C57BL/10) and mdxD2 (DBA2) backgrounds. This enabled the mice to exhibit severe dystrophic histopathology due to the complete lack of dystrophin. They also demonstrated the efficiency of the CRISPR/Cas9 system for exon-skipping in vivo in these newly created hDMD ΔEx45 mice [63]. They electroporated Cas9/gRNA plasmids targeting introns 44 and 55 into the flexor digitorum brevis (FDB) muscle of the mice to induce an in-frame exon 45–55 deletion [63]. Genomic DNA PCR confirmed the successful exons 45–55 deletion in the FDB muscle 22–33 days post-electroporation and dystrophin-positive fibers were revealed by immunostaining. Duchene et al. (2018) created a hybrid exon by connecting exons 47–58 using SaCas9, a therapeutic approach applicable to about 40% of the DMD patients [33]. For in vivo studies, they systemically administered AAV9-mediated delivery of Cas9 and gRNA components in the humanized 33].