A randomly selected extensor digitorum brevis (EDB) muscle in each of three Duchenne muscular dystrophy (DMD) boys aged 9 to 10 was injected with approximately 8 x 106 myoblasts. The contralateral EDBs were sham-injected with carrier solution. Donor myoblasts were derived from cell culture of muscle biopsies from the normal ward or normal brothers of the recipients. Cyclosporine (CsA) treatment began two days before myoblast injection and continued for three months. Three days prior to myoblast injection and three months after, the isometric twitch and maximum voluntary contraction of the left and the right EDBs were measured. Myoblast-injected EDBs showed increases in tensions whereas sham-injected EDBs showed reductions. Both immunocytochemical staining and immunoblot revealed dystrophin in the myoblast-injected EDBs. Dystrophic characteristics such as fiber splitting, central nucleation, phagocytic necrosis, variation in fiber shape and size, and infiltration of fat and connective tissues were less frequently observed in these muscles. Sham-injected EDBs exhibited significant structural and functional degeneration and no dystrophin. Throughout the study, there was no sign of erythema, swelling or tenderness at the injection sites. Serial laboratory evaluation including electrolytes, creatinine, and urea did not reveal any significant changes before or after myoblast transfer. We conclude that myoblast transfer therapy is a safe and efficacious procedure to improve the biochemistry, structure, and function of degenerative EDB muscles in DMD.
Objective: is study was designed to investigate the expression and signi cance of the Forkhead Box M1 (FOXM1) transcription factor in human cervical cancer.Methods: e expression of FOXM1 protein was assessed in tissue microarrays containing 102 cervical cancer tissues by the Streptavidin-Peroxidase (SP) immunohistochemitry technique. e relationship between FOXM1 protein and clinico-pathological features (pathological stages, pathological types, TNM stage) was analyzed.Results: FOXM1 protein was located in the cytoplasma and/or nucleus. e overall expression of FOXM1 in the cytoplasm and nucleus was not associated with T stages (P=0.217) or lymph node status (P=0.313). e nuclear expression of FOXM1 protein was not associated with T stage (P=0.508) or lymph node status (P=0.345). Elevated translocation and activity of FOXM1 were discovered with a secondary analysis that showed that the di erences of the nuclear expression of FOXM1, among di erent pathological stages, were statistically signi cant (P<0.05). e nuclear expression of FOXM1 in low di erential cervical cancer tissues was signi cantly higher than in high di erential cervical cancer tissues (P<0.05).Conclusion: e overexpression of FOXM1 protein in cervical cancer maybe associated with the progression of cervical cancer, and could be a potentially novel tumor marker useful for diagnosis and therapy of cervical cancer.ORIGINAL RESEARCH
Abnormalities in the dystrophic gene product, dystrophin, have been implicated in initiating the primary membrane defect and excessive intracellular calcium accumulation (EICA), which play fundamental pathogenic roles in hereditary muscular dystrophy (HMD). Two other cytoskeletal proteins, spectrin and utrophin, bear remarkable structural and functional homologies to dystrophin. CHF-146 strain dystrophic hamsters (DH), like patients with Duchenne muscular dystrophy (DMD), die prematurely from cardiopulmonary insufficiency, focal myonecrosis, and progressive degeneration of the cardiac and skeletal muscles with EICA. Although DH present a suitable model for HMD, there are controversies concerning their dystrophin and utrophin status. Using immunocytochemistry and Western blotting, we studied dystrophin, spectrin and utrophin anomalies in the cardiac and skeletal muscles of 6-mo-old male DH. Age- and sex-matched CHF-148 strain albino normal hamsters (NH) served as controls. Sarcolemmal dystrophin staining was much weaker and interruptive in the DH. The densitometric analysis of the immunoblots revealed that dystrophin is reduced in DH by 83% in cardiac muscle (p < 0.0001), and by 50% in skeletal muscle (p < 0.0001). We conclude that sarcolemmal dystrophin distribution is markedly reduced and discontinuous in the cardiac and skeletal muscles of DH, with simultaneous upregulation of utrophin and a varied degree of spectrin labelling. This observation suggests that reduced sarcolemmal dystrophin is associated with membrane hyperpermeability, which leads to progressive muscle degeneration via EICA and segmental necrosis in DH. As in DMD, utrophin appears to play an important compensatory role in hamster dystrophinopathy.
A new method is developed using Fluoro-Gold (FG) as a vital stain to label the nuclei of donor myoblasts in myoblast transfer studies. In vitro incubation with 0.01% FG for 16 h resulted in 100% nuclei labelling. Intensive fluorescence persisted following 9 days of subculture, when the human myoblasts were injected into the quadriceps of mouse recipients immunosuppressed with cyclosporine. Injected muscles showed mosaicism of host and donor nuclei 25 days after injection, indicating (i) survival and fusion among donor myoblasts, and (ii) fusion between host and donor cells. FG labelling was not observed in control muscles injected with an equal volume of FG-labelled dead myoblasts, 0.01% FG medium, or phosphate-buffered saline.
In the mean field approximation of nonlinear relativistic σ-ω-ρ model, we have studied the influence of density-dependent coupling constants between nucleons and mesons on the equation of state (EOS) of infinite symmetric nuclear matter in different conditions. We find that the EOS of nuclear matter will become stiffer as c, d in the selfinteraction of σ meson increase when the coefficients except aω in Γω, in which the opposite occurs, are fixed. On the other hand, greater values of aσ, bσ, cσ, aω, dω and smaller values of dσ, bω, cω will lead to stiffer EOS if c and d are fixed. Besides, greater values of Γσ,ω lead to stiffer EOS in high density region for the EOS with same incompressibility coefficient at saturation density.
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