Abstract. When day 1 cultures of chick myogenic cells were exposed to the mutagenic alkylating agent ethyl methanesulfonate (EMS) for 3 d, 80% of the replicating cells were killed, but postmitotic myoblasts survived. The myoblasts fused to form unusual multinucleated "myosheets": extraordinarily wide, flattened structures that were devoid of myofibrils but displayed extensive, submembranous stress fiber-like structures (SFLS). Immunoblots of the myosheets indicated that the carcinogen blocked the synthesis and accumulation of the myofibrillar myosin isoforms but not that of the cytoplasmic myosin isoform.When removed from EMS, widely spaced nascent myofibrils gradually emerged in the myosheets after 3 d. Striking co-localization of fluorescent reagents that stained SFLS and those that specifically stained myofibrils was observed for the next 2 d, By both immunofluorescence and electron microscopy, individual nascent myofibrils appeared to be part of, or juxtaposed to, preexisting individual SFLS. By day 6, all SFLS had disappeared, and the definitive myofibrils were displaced from their submembranous site into the interior of the myosheet. Immunoblots from recovering myosheets demonstrated a temporal correlation between the appearance of the myofibrillar myosin isoforms and the assembly of thick filaments. The assembly of definitive myofibrils did not appear to involve desmin intermediate filaments, but a striking aggregation of sarcoplasmic reticulum elements was seen at the level of each I-Z-band. Our findings suggest that SFLS in the EMS myosheets function as early, transitory assembly sites for nascent myofibrils.EFINITIVE muscle cells selectively synthesize a complex set of contractile proteins that interact precisely to form the relatively invariant striated myofibril. Major myofibrillar components include muscle-specific isoforms such as myosin heavy and light chains, alpha-actin, tropomyosins, troponins, alpha-actinin, titin, nebulin, and M-band proteins (see articles cited in reference 52). These myofibrillar isoforms are synthesized and assembled into definitive sarcomeres arranged in tandem during the earliest stages of myofibrillogenesis in vivo and in vitro (2, 21, 33). With maturation there is an enormous increase in the numbers ofinterdigitating thick and thin filaments in each nascent myofibril, the total number of individual myofibrils, and the number of new sarcomeres, which apparently are added at the ends of the elongating myofibrils (1,14,31,33,36, 68).An intriguing aspect of myofibrillogenesis is that many of the muscle-specific isoforms correspond to a related set of proteins that are synthesized in virtually all cells, including presumptive myoblasts, chondroblasts, nerve cells, fibroblasts, and endothelial cells. In nonmuscle cells these constitutive contractile protein isoforms are not present in a stable arrangement but may interact to form stress fibers and/or microfilaments, depending upon the degree of cell spreading, motility, attachment to the substrate, and hemodynamic factors (2...
The proportions of fast and slow myosin molecules in external urethral sphincter specimens from ten urodynamically normal male bladder carcinoma patients were estimated from the contents of fast and slow myosin light chains in two-dimensional electrophoretic gels. The percentages of fast and slow myosin molecules ranged from 5.0% to 61.4% with a mean of 35.5% and from 38.6% to 95.0% with a mean of 65.5% respectively. It is therefore concluded that the human external urethral sphincter is composed of both fast and slow muscle fibers as well as other voluntary muscles. The human external urethral sphincter is considered to be a highly fatigue-resistant muscle with a very high proportion of slow muscle fibers. In the cases studied so far, there is a great diversity in the proportions of fast and slow myosin molecules; the reason for this remains unknown.
We report our experience with 17 cases of paraureteral diverticula seen in the last 12 years. These 17 cases represent a particular group of patients with ureteral reflux in that they often had ureteral obstruction too. Early operative intervention is recommended. There is a trend towards renal dysmorphism and dysplasia as the position of the ureteral orifice laterlizes in the diverticulum. A paraureteral diverticulum was considered to be the developmental extravesical expansion of the terminal ureteral end by virtue of the caudally positioned ureteral bud in the wolffian duct.
The structures of the ureter, ureterovesical junction, bladder and sphincteric urethra were investigated histologically in 17 human fetuses (from 3rd to 21st weeks) and 2 neonates, with particular emphasis on their muscular development. The differentiation of ureteral muscle begins from the upper part of the ureter at the 12th week and muscle bundles run spirally. The purely longitudinal intramural ureteral muscle differentiates much later than the upper ureteral muscle and begins to form muscle bundles at the 17th week. The deep periureteral sheath and the trigonal muscle differentiate at an almost similar pace to the intramural ureteral muscle. The detrusor muscle begins to differentiate from the apical dome of the bladder at the 7th week. Distinct superficial periureteral sheath is also seen around the 12th week. The urethral striated muscle is recognized at the 8th week. It starts to develop in the anterior wall of the urethra as a dense cellular accumulation which eventually extends caudolaterally to form a U-shaped figure. The urethral smooth muscle starts its differentiation between the 9th and 11th weeks inside the urethral striated muscle.
We report on 17 female and 4 male patients with single ectopic ureters, 9 of whom also had vaginal ectopic ureters. The clinicopathological features and surgical management are presented, with particular emphasis on the associated renal dysplasia and the complete excision of the ectopic ureteral stump. Although single ureteral ectopia with drainage to the vagina is rare in the English literature the condition is common in Japan.
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