Clinically Differentiated Abnormalities of the Architecture and Expression of Myosin Isoforms of the Human Cremaster Muscle in Cryptorchidism and Retractile Testis

2020 ◽  
Vol 104 (11-12) ◽  
pp. 891-901
Author(s):  
Francesco Molinaro ◽  
Giulia Fusi ◽  
Margherita Aglianò ◽  
Nila Volpi ◽  
Daniela Franci ◽  
...  
Keyword(s):  
Striated Muscle ◽  
Masticatory Muscles ◽  
The Other ◽  
Molecular Characteristics ◽  
Testicular Descent ◽  
Myosin Isoforms ◽  
Cremaster Muscle ◽  
Muscle Groups ◽  
Retractile Testis ◽  
Gubernaculum Testis

<b><i>Aim:</i></b> To describe architecture and expression of myosin isoforms of the human cremaster muscle (CM) and to individuate changes in clinically differentiated abnormalities of testicular descent: cryptorchidism or undescended testis (UDT) and retractile testis (RT). <b><i>Background:</i></b> The CM is a nonsomitic striated muscle differentiating from mesenchyme of the gubernaculum testis. Morphofunctional and molecular peculiarities linked to its unique embryological origin are not yet completely defined. Its role in abnormalities of testicular descent is being investigated. <b><i>Subjects and Methods:</i></b> Biopsy samples were obtained from corrective surgery in cases of cryptorchidism, retractile testis, inguinal hernia, or hydrocele. Muscle specimens were processed for morphology, histochemistry, and immunohistology. <b><i>Results and Conclusions:</i></b> The CM differs from the skeletal muscles both for morphological and molecular characteristics. The presence of fascicles with different characterization and its myosinic pattern suggested that the CM could be included in the specialized muscle groups, such as the extrinsic ocular muscles (EOMs) and laryngeal and masticatory muscles. The embryological origin from the nonsomitic mesoderm is, also for the CM, the basis of distinct molecular pathways. In UDT, the histological alterations of CM are suggestive of denervation; the genitofemoral nerve and its molecular messengers directed to this muscle are likely defective. Compared with the other samples, RT has a distinct myosinic pattern; therefore, it has been considered a well-defined entity with respect to the other testicular descent abnormalities.

Chronic GnRH administration in prepubertal male pigs

1988 ◽  
Vol 118 (1) ◽  
pp. 109-118 ◽  
Author(s):  
Grietje Dijkstra ◽  
J. Martje Fentener van Vlissingen ◽  
C. J. G. Wensing ◽  
P. M. M. van Dorst-Bruijns ◽  
H.J. Degenhart ◽  
...  
Keyword(s):  
Low Dose ◽  
The Other ◽  
Testicular Descent ◽  
Dependent Manner ◽  
Cremaster Muscle ◽  
Histological Changes ◽  
Treatment Dose ◽  
Basal Plasma ◽  
Plasma Hormone ◽  
Dose Dependent

Abstract. The effect of chronic pulsatile low-dose GnRH treatment on the juvenile testis and associated structures was evaluated in relation to hormonal parameters in the peripheral blood in the pig. Starting at 8 weeks of age, male pigs (crossbreds of Dutch Landrace and Yorkshire breeds) were injected 6 times daily im with 0, 75 or 250 ng GnRH/kg body weight during 4 weeks. Immediately after the treatment period, a GnRH stimulation test with 750 ng GnRH/kg iv was carried out. Samples for plasma LH, FSH, testosterone and 5αDHT measurement were obtained weekly (basal level) and after GnRH stimulation. The pigs were castrated at 12 weeks of age and the weights and lengths of the testis, epididymis and cremaster muscle were recorded. Intratesticular testosterone and 5αDHT concentrations were determined, and the testis and epididymis were evaluated for histological changes. Basal plasma hormone concentrations, intratesticular androgen concentrations and the response of the pituitary gland to stimulation had not been affected by GnRH treatment. Pigs receiving the higher treatment dose of GnRH showed less increase in testosterone levels in response to the stimulation dose at 12 weeks of age than the other pigs. Morphologically, no changes were observed in the epididymis and cremaster muscle after GnRH treatment and no signs of reactivation of structures that can provoke testicular descent could be seen. The development of the seminiferous epithelium was more advanced in the GnRH-treated groups, apparently in a dose-dependent manner.

Consultation with the specialist

1994 ◽  
Vol 15 (7) ◽  
pp. 272-274
Author(s):  
Ronald Rabinowitz ◽  
William C. Hulbert
Keyword(s):  
Single Gene ◽  
Testicular Descent ◽  
Term Infants ◽  
Genital Abnormality ◽  
John Hunter ◽  
Multiple Malformation ◽  
Gene Defects ◽  
Definition Of ◽  
Retractile Testis ◽  
Malformation Syndromes

Introduction The term cryptorchidism originates from the Greek kryptos (concealed) and orchis (testis). The definition of the term cryptorchidism is appropriate; not only is the testis concealed, but so is much information regarding this common condition. More than 200 years ago, John Hunter described descent of the testis during the last 3 months of gestation and reported that testes that remain in the abdomen are unhealthy and do not function well. He also discussed the possibilities of failure to descend causing testicular abnormality and testicular abnormalities causing failure to descend. Cryptorchidism represents the most common genital abnormality seen by pediatric urologists. The incidence is 1 in 125 boys. The incidence is much higher in premature infants (1 in 3), and the lower the birth weight, the greater the incidence of cryptorchidism. This condition is seen in approximately 1 in 30 full-term infants, but in many of them, the testicles will descend during the first few months of life. There is a higher incidence of cryptorchidism associated with many chromosomal and single gene defects as well as with multiple malformation syndromes. In addition, there is a higher incidence of cryptorchidism in the siblings and sons of those who have or had cryptorchidism. We will describe the anatomy of both the cryptorchid and retractile testis and discuss the embryology of testicular descent, with an emphasis on hormonal factors.

The Dogfish Neuromuscular Junction: Dual Innervation of Vertebrate Striated Muscle Fibres?

1972 ◽  
Vol 10 (3) ◽  
pp. 657-665
Author(s):  
Q. BONE
Keyword(s):  
Neuromuscular Junction ◽  
Nerve Terminal ◽  
Striated Muscle ◽  
Dense Core ◽  
The Other ◽  
Muscle Fibres ◽  
Nerve Terminals ◽  
Nerve Fibres ◽  
Different Types ◽  
Motor End Plate

In the myotomal muscles of the dogfish, Scyliorhinu canicula, there are 2 major types of fibre. The red fibres at the periphery of the myotome receive a distributed en grappe pattern of innervation. There are subjunctional folds at these endings, and the nerve terminals contain vesicles around 50 nm in diameter. In contrast to this, the white twitch fibres of the myotome are innervated focally, by 2 nerve fibres passing to the same motor end-plate. These 2 fibres contain vesicles of different types. One type of nerve terminal contains vesicles around 50 nm in diameter; these terminals resemble those upon the red fibres. The other contains vesicles up to 100 nm in diameter, frequently possessing a dense core. It is suggested that the white twitch fibres of dogfish are innervated by 2 separate axons, possibly containing different transmitter substances.

Effect of cellular determination on oncogenic transformation by chemicals and oncogenes

1988 ◽  
Vol 8 (10) ◽  
pp. 4322-4327
Author(s):  
M A Harrington ◽  
F Gonzales ◽  
P A Jones
Keyword(s):  
Striated Muscle ◽  
Myogenic Differentiation ◽  
Cell Types ◽  
Soft Agar ◽  
The Other ◽  
Ras Oncogene ◽  
Oncogenic Transformation ◽  
Ras Gene ◽  
Embryo Cells ◽  
End Stage

Three developmentally determined myogenic cell lines derived from C3H 10T1/2 C18 (10T1/2) mouse embryo cells treated with 5-azacytidine were compared with the parental 10T1/2 line for their susceptibility to oncogenic transformation by 3-methylcholanthrene or the activated human c-Ha-ras oncogene. Neither the 10T1/2 cells nor the myogenic derivatives grew in soft agar or formed tumors in nude mice. In contrast to 10T1/2 cells, the three myogenic derivatives were not susceptible to transformation by 3-methylcholanthrene, so that cellular determination altered the response of 10T1/2 cells to chemical carcinogen. On the other hand, all cell types were transformed to a tumorigenic phenotype following transfection with the activated c-Ha-ras gene. The transfected myogenic cells expressed both the c-Ha-ras gene and the muscle determination gene MyoD1. In contrast to other reports, the presence of as many as six copies of the c-Ha-ras gene per genome did not prevent the formation of striated muscle cells which expressed immunologically detectable muscle-specific myosin. The expression of the c-Ha-ras gene does not therefore necessarily preclude the expression of the determination gene for myogenesis or prevent end-stage myogenic differentiation.

Contribution of adenosine to arteriolar autoregulation in striated muscle

1983 ◽  
Vol 244 (4) ◽  
pp. H567-H576 ◽  
Author(s):  
R. J. Morff ◽  
H. J. Granger
Keyword(s):  
Blood Flow ◽  
Striated Muscle ◽  
Perfusion Pressure ◽  
Cremaster Muscle ◽  
Sprague Dawley ◽  
Red Blood Cell Velocity ◽  
Myogenic Factors ◽  
Bath Medium ◽  
Arteriolar Diameter

The contribution of adenosine to blood flow autoregulation in striated muscle was evaluated by direct in vivo visualization of arterioles in the rat cremaster muscle. Male Sprague-Dawley rats were anesthetized with pentobarbital sodium, and the cremaster muscle was surgically exposed and maintained in a controlled tissue bath environment with pH 7.40, CO2 tension (PCO2) congruent to 40 mmHg, and O2 tension (PO2) at either a high (congruent to 70 mmHg) or a low (congruent to 10 mmHg) value. Local adenosine activity was blocked in some animals by the addition of theophylline (3 X 10(-5) M) to the bath medium. Individual second (2A)- and third (3A)-order arterioles were observed via closed-circuit television microscopy, and blood flow in each arteriole was calculated from simultaneous measurements of arteriolar diameter and red blood cell velocity. Perfusion pressure to the animal's hindquarters was altered by varying the degree of occlusion of the sacral aorta; arteriolar diameter, velocity, and blood flow responses were plotted as a function of the varying pressure. Both 2A and 3A arterioles exhibited vasodilation and substantial superregulation of blood flow (increased blood flow with decreased perfusion pressure) when bath PO2 was low and adenosine activity was not blocked. Addition of theophylline to the cremaster bath medium significantly reduced the dilation and abolished superregulation, although substantial autoregulation remained. When bath PO2 was high, the degree of arteriolar dilation and autoregulation was reduced compared with the low bath PO2 responses, and blocking adenosine activity had no effect on the responses. These results support the concept that changes in local adenosine levels are involved in the autoregulatory responses observed in the rat cremaster muscle and that the magnitude of adenosine's contribution is directly related to the degree of tissue hypoxia. However, blocking adenosine activity did not totally abolish autoregulation, suggesting that other metabolic and/or myogenic factors may also be contributing to blood flow regulation in this tissue.

scholarly journals Cellular and Animal Models of Striated Muscle Laminopathies

Cells ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. 291 ◽  
Author(s):  
Hannah A. Nicolas ◽  
Marie-Andrée Akimenko ◽  
Frédérique Tesson
Keyword(s):  
Skeletal Muscle ◽  
Skeletal Muscles ◽  
Molecular Mechanisms ◽  
Striated Muscle ◽  
Nuclear Lamina ◽  
The Other ◽  
Lamin A ◽  
Lmna Gene ◽  
Future Directions ◽  
Exon 10

The lamin A/C (LMNA) gene codes for nuclear intermediate filaments constitutive of the nuclear lamina. LMNA has 12 exons and alternative splicing of exon 10 results in two major isoforms—lamins A and C. Mutations found throughout the LMNA gene cause a group of diseases collectively known as laminopathies, of which the type, diversity, penetrance and severity of phenotypes can vary from one individual to the other, even between individuals carrying the same mutation. The majority of the laminopathies affect cardiac and/or skeletal muscles. The underlying molecular mechanisms contributing to such tissue-specific phenotypes caused by mutations in a ubiquitously expressed gene are not yet well elucidated. This review will explore the different phenotypes observed in established models of striated muscle laminopathies and their respective contributions to advancing our understanding of cardiac and skeletal muscle-related laminopathies. Potential future directions for developing effective treatments for patients with lamin A/C mutation-associated cardiac and/or skeletal muscle conditions will be discussed.

Benign Gastrointestinal Mesenchymal BUMPS: A Brief Review of Some Spindle Cell Polyps With Published Names

2011 ◽  
Vol 135 (10) ◽  
pp. 1311-1319 ◽  
Author(s):  
Ahren C Rittershaus ◽  
Henry D Appelman
Keyword(s):  
Schwann Cell ◽  
Spindle Cell ◽  
Granular Cell ◽  
The Other ◽  
Data Sources ◽  
Molecular Characteristics ◽  
Muscularis Mucosae ◽  
Endoscopic Biopsies ◽  
Inflammatory Fibroid Polyps

Context.—There are several benign, predominantly spindle cell, mesenchymal proliferations involving the mucosa and/or submucosa in the gut, which present as polyps and pathologists see as polypectomy specimens. These include perineuriomas, Schwann cell nodules, ganglioneuromas, leiomyomas of the muscularis mucosae, inflammatory fibroid polyps, and granular cell tumors. Objectives.—To evaluate these mesenchymal polyps for their morphologic, immunohistochemical, ultrastructural, and molecular characteristics and to determine some of their associations. Data Sources.—Personal observations based on years of analyzing endoscopic biopsies and a review of the world's literature. Conclusions.—These polyps do surface every so often. There is significant literature covering inflammatory fibroid polyps and granular cell tumors, but there is little literature about the other entities.

An insight into testis and gubernaculum dynamics of INSL3 - RXFP2 signalling during testicular descent in the dog

2010 ◽  
Vol 22 (5) ◽  
pp. 751 ◽  
Author(s):  
S. Arrighi ◽  
G. Bosi ◽  
D. Groppetti ◽  
M. Aralla ◽  
F. Cremonesi
Keyword(s):  
Sertoli Cells ◽  
Leydig Cells ◽  
Feedback Loop ◽  
Testicular Descent ◽  
Fetal Period ◽  
Male Development ◽  
Dog Testis ◽  
Gubernaculum Testis ◽  
Insight Into ◽  
Different Tissues

Insulin-like 3 (INSL3) plays a prominent role in male development and is supposed to induce the growth of the gubernaculum testis (g.t.), thus being directly involved in testicular descent in humans and rodents. This happens through activation of the RXFP2 receptor (GREAT or LGR8). The INSL3–RXFP2 complex is reputed to play an additional paracrine role in the testis, possibly acting as part of an autocrine feedback loop. The present work provides evidence of the immunolocalisation of INSL3 in the Leydig cells of canine fetuses and of the expression of RXFP2 receptor in different tissues of the g.t. of the same specimens. RXFP2 was localised at the cell membrane of g.t. muscle and connective cells, as well as in the epithelial cells of the developing excurrent ducts. Notably, RXFP2 immunoreactivity of the g.t. was limited to fetuses at ~35–45 days of gestation, which is also the fetal period when the endocrine compartment of the dog testis is active endocrinologically, as confirmed by the anti-P450c17 and anti-INSL3 immunoreactivities of the fetal Leydig cells, and by anti-Müllerian hormone immunoreactivity of the Sertoli cells. The same immunoreactivities were also evaluated in the testes of cryptorchid dogs of different ages. RXFP2 immunoreactivity was absent from genital tracts of cryptorchid testes and g.t. remnants.

scholarly journals THE DOUBLE ARRAY OF FILAMENTS IN CROSS-STRIATED MUSCLE

1957 ◽  
Vol 3 (5) ◽  
pp. 631-648 ◽  
Author(s):  
H. E. Huxley
Keyword(s):  
Striated Muscle ◽  
The Other ◽  
Thin Sections ◽  
Alternative Models ◽  
Double Array ◽  
The Cross ◽  
Cross Bridges

The conditions under which one might expect to see the secondary filaments (if they exist) in longitudinal sections of striated muscle, are discussed. It is shown that these conditions were not satisfied in previously published works for the sections were too thick. When suitably thin sections are examined, the secondary filaments can be seen perfectly easily. It is also possible to see clearly other details of the structure, notably the cross-bridges between primary and secondary filaments, and the tapering of the primary filaments at their ends. The arrangement of the filaments and the changes associated with contraction and with stretch are identical to those already deduced from previous observations and described in terms of the interdigitating filament model in previous papers. There are therefore excellent grounds for believing that this model is correct. The alternative models which have been proposed appear to be incompatible both with the present observations and with much of the other available evidence.

scholarly journals Molecular characteristics of papillary thyroid carcinomas without BRAF mutation or RET/PTC rearrangement: relationship with clinico-pathological features

2009 ◽  
Vol 16 (2) ◽  
pp. 467-481 ◽  
Author(s):  
Stéphanie Durand ◽  
Carole Ferraro-Peyret ◽  
Mireille Joufre ◽  
Annie Chave ◽  
Françoise Borson-Chazot ◽  
...  
Keyword(s):  
Gene Expression ◽  
Normal Tissue ◽  
Expression Profiles ◽  
Strong Association ◽  
The Other ◽  
Marker Genes ◽  
Molecular Characteristics ◽  
Papillary Thyroid ◽  
Thyroid Carcinomas ◽  
Gene Alteration

About 60–70% of papillary thyroid carcinomas (PTC) present a BRAFT1799A gene mutation or a rearrangement of RET gene (RET/PTC). In this study, we examined whether PTC without BRAFT1799A mutation and without RET/PTC rearrangement named PTC-ga(−) were distinguishable from PTC-ga(+) (with one or the other gene alteration) on the basis of gene expression characteristics. We analyzed the mutational state of 116 PTC and we compared gene expression profiles of PTC-ga(+) and PTC-ga(−) from data of a 200 gene macroarray and quantitative PCR. Seventy five PTC were PTC-ga(+) and 41 were PTC-ga(−). Unsupervised analyses of macroarray data by hierarchical clustering led to a complete segregation of PTC-ga(+) and PTC-ga(−). In a series of 42 genes previously recognized as PTC ‘marker’ genes, 22 were found to be expressed at a comparable level in PTC-ga(−) and normal tissue. Thyroid-specific genes, TPO, TG, DIO1, and DIO2 were under-expressed in PTC-ga(+) but expressed at a normal level in PTC-ga(−). A few genes including DUOX1 and DUOX2 were selectively dys-regulated in PTC-ga(−). Tumor grade of PTC-ga(−) was lower than that of PTC-ga(+). There was a strong association between the mutational state and histiotype of PTC; 81% of PTC follicular variants were corresponded to PTC-ga(−), whereas 84% of PTC of classical form were PTC-ga(+). In conclusion, we show that PTC without BRAFT1799A mutation or RET/PTC rearrangement, mainly corresponding to follicular variants, maintain a thyroid differentiation expression level close to that of normal tissue and should be of better prognosis than PTC with one or the other gene alteration.

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