scholarly journals Congenital muscle dystrophy and diet consistency affect mouse skull shape differently

2017 ◽  
Vol 231 (5) ◽  
pp. 736-748 ◽  
Author(s):  
Alexander Spassov ◽  
Viviana Toro-Ibacache ◽  
Mirjam Krautwald ◽  
Heinrich Brinkmeier ◽  
Kornelius Kupczik
Keyword(s):  
Muscle Dystrophy ◽  
Skull Shape ◽  
Diet Consistency

scholarly journals Skull shape of a widely distributed, endangered marsupial reveals little evidence of local adaptation between fragmented populations

2020 ◽  
Vol 10 (18) ◽  
pp. 9707-9720
Author(s):  
Pietro Viacava ◽  
Simone P. Blomberg ◽  
Gabriele Sansalone ◽  
Matthew J. Phillips ◽  
Thomas Guillerme ◽  
...  
Keyword(s):  
Local Adaptation ◽  
Fragmented Populations ◽  
Skull Shape

scholarly journals Evolution and expansion of the RUNX2 QA repeat corresponds with the emergence of vertebrate complexity

2020 ◽  
Vol 3 (1) ◽  
Author(s):  
Axel H. Newton ◽  
Andrew J. Pask
Keyword(s):  
Natural Variation ◽  
Skeletal Development ◽  
Skull Shape ◽  
Morphological Novelty ◽  
Transactivation Potential ◽  
Repeat Domain ◽  
Related Transcription Factor ◽  
Mammalian Skull ◽  
Evolutionary Tuning

AbstractRunt-related transcription factor 2 (RUNX2) is critical for the development of the vertebrate bony skeleton. Unlike other RUNX family members, RUNX2 possesses a variable poly-glutamine, poly-alanine (QA) repeat domain. Natural variation within this repeat is able to alter the transactivation potential of RUNX2, acting as an evolutionary ‘tuning knob’ suggested to influence mammalian skull shape. However, the broader role of the RUNX2 QA repeat throughout vertebrate evolution is unknown. In this perspective, we examine the role of the RUNX2 QA repeat during skeletal development and discuss how its emergence and expansion may have facilitated the evolution of morphological novelty in vertebrates.

scholarly journals Pattern and pace of morphological change due to variable human impact: the case of Japanese macaques

Primates ◽  
2021 ◽  
Author(s):  
Madeleine Geiger
Keyword(s):  
Body Size ◽  
Human Impact ◽  
Morphological Variation ◽  
Japanese Macaques ◽  
Linear Measurements ◽  
Skull Shape ◽  
Rates Of Change ◽  
Animal Populations ◽  
Captive Populations ◽  
In Captivity

AbstractHuman impact influences morphological variation in animals, as documented in many captive and domestic animal populations. However, there are different levels of human impact, and their influence on the pattern and rate of morphological variation remains unclear. This study contributes to the ongoing debate via the examination of cranial and mandibular shape and size variation and pace of change in Japanese macaques (Macaca fuscata). This species is ideal for tackling such questions because different wild, wild-provisioned, and captive populations have been monitored and collected over seven decades. Linear measurements were taken on 70 skulls from five populations, grouped into three ‘human impact groups’ (wild, wild-provisioned, and captive). This made it possible to investigate the pattern and pace of skull form changes among the human impact groups as well as over time within the populations. It was found that the overall skull shape tends to differ among the human impact groups, with captive macaques having relatively longer rostra than wild ones. Whether these differences are a result of geographic variation or variable human impact, related to nutritional supply and mechanical properties of the diet, is unclear. However, this pattern of directed changes did not seem to hold when the single captive populations were examined in detail. Although environmental conditions have probably been similar for the two examined captive populations (same captive locality), skull shape changes over the first generations in captivity were mostly different. This varying pattern, together with a consistent decrease in body size in the captive populations over generations, points to genetic drift playing a role in shaping skull shape and body size in captivity. In the captive groups investigated here, the rates of change were found to be high compared to literature records from settings featuring different degrees of human impact in different species, although they still lie in the range of field studies in a natural context. This adds to the view that human impact might not necessarily lead to particularly fast rates of change.

scholarly journals Quantitative Assessment of Shape Deformation of Regional Cranial Bone for Evaluation of Surgical Effect in Patients with Craniosynostosis

2021 ◽  
Vol 11 (3) ◽  
pp. 990
Author(s):  
Min Jin Lee ◽  
Helen Hong ◽  
Kyu Won Shim
Keyword(s):  
Quantitative Assessment ◽  
Deformable Registration ◽  
Occipital Bone ◽  
Cranial Bone ◽  
Shape Deformation ◽  
Surface Model ◽  
Cephalic Index ◽  
Skull Shape ◽  
Quantification Method ◽  
Parietal Bones

Surgery in patients with craniosynostosis is a common treatment to correct the deformed skull shape, and it is necessary to verify the surgical effect of correction on the regional cranial bone. We propose a quantification method for evaluating surgical effects on regional cranial bones by comparing preoperative and postoperative skull shapes. To divide preoperative and postoperative skulls into two frontal bones, two parietal bones, and the occipital bone, and to estimate the shape deformation of regional cranial bones between the preoperative and postoperative skulls, an age-matched mean-normal skull surface model already divided into five bones is deformed into a preoperative skull, and a deformed mean-normal skull surface model is redeformed into a postoperative skull. To quantify the degree of the expansion and reduction of regional cranial bones after surgery, expansion and reduction indices of the five cranial bones are calculated using the deformable registration as deformation information. The proposed quantification method overcomes the quantification difficulty when using the traditional cephalic index(CI) by analyzing regional cranial bones and provides useful information for quantifying the surgical effects of craniosynostosis patients with symmetric and asymmetric deformities.

scholarly journals Urinary Titin N-Fragment as a Biomarker of Muscle Atrophy, Intensive Care Unit-Acquired Weakness, and Possible Application for Post-Intensive Care Syndrome

2021 ◽  
Vol 10 (4) ◽  
pp. 614 ◽  
Author(s):  
Nobuto Nakanishi ◽  
Rie Tsutsumi ◽  
Kanako Hara ◽  
Masafumi Matsuo ◽  
Hiroshi Sakaue ◽  
...  
Keyword(s):  
Intensive Care Unit ◽  
Intensive Care ◽  
Muscle Atrophy ◽  
Critically Ill Patients ◽  
Chronic Illnesses ◽  
Rehabilitation Management ◽  
Muscle Dystrophy ◽  
Thin Filaments ◽  
Thick Filaments ◽  
Post Intensive Care Syndrome

Titin is a giant protein that functions as a molecular spring in sarcomeres. Titin interconnects the contraction of actin-containing thin filaments and myosin-containing thick filaments. Titin breaks down to form urinary titin N-fragments, which are measurable in urine. Urinary titin N-fragment was originally reported to be a useful biomarker in the diagnosis of muscle dystrophy. Recently, the urinary titin N-fragment has been increasingly gaining attention as a novel biomarker of muscle atrophy and intensive care unit-acquired weakness in critically ill patients, in whom titin loss is a possible pathophysiology. Furthermore, several studies have reported that the urinary titin N-fragment also reflected muscle atrophy and weakness in patients with chronic illnesses. It may be used to predict the risk of post-intensive care syndrome or to monitor patients’ condition after hospital discharge for better nutritional and rehabilitation management. We provide several tips on the use of this promising biomarker in post-intensive care syndrome.

scholarly journals Autophagy induction in atrophic muscle cells requires ULK1 activation by TRIM32 through unanchored K63-linked polyubiquitin chains

2019 ◽  
Vol 5 (5) ◽  
pp. eaau8857 ◽  
Author(s):  
M. Di Rienzo ◽  
M. Antonioli ◽  
C. Fusco ◽  
Y. Liu ◽  
M. Mari ◽  
...  
Keyword(s):  
Mouse Models ◽  
Muscle Atrophy ◽  
Ubiquitin Ligase ◽  
Muscle Dystrophy ◽  
Polyubiquitin Chains ◽  
Autophagy Induction ◽  
Atrophic Muscle ◽  
Autophagic Activity

Optimal autophagic activity is crucial to maintain muscle integrity, with either reduced or excessive levels leading to specific myopathies. LGMD2H is a muscle dystrophy caused by mutations in the ubiquitin ligase TRIM32, whose function in muscles remains not fully understood. Here, we show that TRIM32 is required for the induction of muscle autophagy in atrophic conditions using both in vitro and in vivo mouse models. Trim32 inhibition results in a defective autophagy response to muscle atrophy, associated with increased ROS and MuRF1 levels. The proautophagic function of TRIM32 relies on its ability to bind the autophagy proteins AMBRA1 and ULK1 and stimulate ULK1 activity via unanchored K63-linked polyubiquitin. LGMD2H-causative mutations impair TRIM32’s ability to bind ULK1 and induce autophagy. Collectively, our study revealed a role for TRIM32 in the regulation of muscle autophagy in response to atrophic stimuli, uncovering a previously unidentified mechanism by which ubiquitin ligases activate autophagy regulators.

scholarly journals Glu20Ter Variant in PLEC 1f Isoform Causes Limb-Girdle Muscle Dystrophy with Lung Injury

2017 ◽  
Vol 8 ◽  
Author(s):  
Roman V. Deev ◽  
Sergei N. Bardakov ◽  
Mikhail O. Mavlikeev ◽  
Ivan A. Yakovlev ◽  
Zoya R. Umakhanova ◽  
...  
Keyword(s):  
Lung Injury ◽  
Muscle Dystrophy ◽  
Girdle Muscle

A prepotent factor in the determination of skull shape

1934 ◽  
Vol 54 (2) ◽  
pp. 333-346 ◽  
Author(s):  
J. A. Dye ◽  
F. S. Kinder
Keyword(s):  
Skull Shape

P.8.1 Muscle biopsy findings in Limb Girdle muscle Dystrophy 2I (LGMD2I)

2013 ◽  
Vol 23 (9-10) ◽  
pp. 779-780
Author(s):  
S. Lindal ◽  
K. Myreng ◽  
S. Løseth ◽  
C. Jonsrud ◽  
M. Alhamidi ◽  
...  
Keyword(s):  
Muscle Biopsy ◽  
Muscle Dystrophy ◽  
Girdle Muscle
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