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[en] Soft tissue sarcomas comprise approximately 1% of malignant tumors. There are more than 50 subtypes, but pleomorphic sarcoma, liposarcoma, leiomyosarcoma, synovial sarcoma, and malignant peripheral nerve sheath tumor account for 75%. Differentiation between these subtypes is difficult because they often present with a painless enlarging mass, and share many histological and MR imaging features. Nonetheless, subdifferentiation is important because the different subtypes have different prognoses and therapeutic strategies. In this manuscript we discuss the clinical, histological, and MR imaging features of soft tissue sarcomas according to the WHO classification. An overview is provided and differentiating features are discussed that can help to narrow down the differential diagnosis. (orig.)
[en] Lamin A is a nuclear lamina constituent implicated in a number of human disorders including Emery-Dreifuss muscular dystrophy. Since increasing evidence suggests a role of the lamin A precursor in nuclear functions, we investigated the processing of prelamin A during differentiation of C2C12 mouse myoblasts. We show that both protein levels and cellular localization of prelamin A are modulated during myoblast activation. Similar changes of lamin A-binding proteins emerin and LAP2α were observed. Furthermore, prelamin A was found in a complex with LAP2α in differentiating myoblasts. Prelamin A accumulation in cycling myoblasts by expressing unprocessable mutants affected LAP2α and PCNA amount and increased caveolin 3 mRNA and protein levels, while accumulation of prelamin A in differentiated muscle cells following treatment with a farnesyl transferase inhibitor appeared to inhibit caveolin 3 expression. Our data provide evidence for a critical role of the lamin A precursor in the early steps of muscle cell differentiation
[en] A descriptive, retrospective study of patients with histopathologic diagnosis of basal cell carcinoma, squamous cell and adenocarcinoma of sebaceous glands, assisted in the service of oculoplasty the Cuban Institute of Ophthalmology January 2005 to December 2010. It was included 109 patients; we analyzed age, sex, skin color, clinical symptoms, anatomic location, degree of cell differentiation and annual basis
[en] The inhibition of E2F has been demonstrated to be important in the initiation of squamous differentiation by two independent manners: promotion of growth arrest and the relief of the differentiation-suppressive properties of E2Fs. E2F6 is reported to behave as a transcriptional repressor of the E2F family. In this study, we examined the ability of E2F6 to act as the molecular switch required for E2F inhibition in order for keratinocytes to enter a terminal differentiation programme. Results demonstrated that whilst E2F6 was able to suppress E2F activity in proliferating keratinocytes, it did not modulate squamous differentiation in a differentiated keratinocyte. Furthermore, inhibition of E2F, by overexpressing E2F6, was not sufficient to sensitise either proliferating keratinocytes or the squamous cell carcinoma cell line, KJD-1/SV40, to differentiation-inducing agents. Significantly, although E2F6 could suppress E2F activity in proliferating cells, it could not inhibit proliferation of KJD-1/SV40 cells. These results demonstrate that E2F6 does not contain the domains required for modulation of squamous differentiation and imply isoform-specific functions for individual E2F family members
[en] In myotonic dystrophy type I (DM1), nuclear retention of mutant DMPK transcripts compromises muscle cell differentiation. Although several reports have identified molecular defects in myogenesis, it remains still unclear how exactly the retention of the mutant transcripts induces this defect. We have recently created a novel cellular model in which the mutant DMPK 3' UTR transcripts were released to the cytoplasm of myoblasts by using the WPRE genetic element. As a result, muscle cell differentiation was repaired. In this paper, this cellular model was further exploited to investigate the effect of the levels and location of the mutant transcripts on muscle differentiation. Results show that the levels of these transcripts were proportional to the inhibition of both the initial fusion of myoblasts and the maturity of myotubes. Moreover, the cytoplasmic export of the mutant RNAs to the cytoplasm caused less inhibition only in the initial fusion of myoblasts.
[en] To prospectively evaluate magnetic resonance (MR) imaging including dynamic contrast-enhanced MR imaging in the differentiation of benign from malignant orbital masses and to evaluate which MR imaging features are most predictive of malignant tumors. The study was approved by the institutional review board and signed informed consent was obtained. Nonenhanced, static, and dynamic contrast-enhanced MR imaging was performed in 102 adult patients with an orbital mass. Diagnosis was based on histologic findings. MR imaging features of benign and malignant orbital lesions were evaluated correlated with histological findings. Multivariate logistic regression analysis was employed to identify the best combination of MR imaging features that might be predictive of malignancy. Nonenhanced, static, and dynamic enhancement MR imaging was significantly superior to two other models in prediction of malignancy (p < 0.05). Multivariate logistic regression analysis identified that the most discriminating MR imaging features were isointense mass on T2-weighted imaging and a washout-type time-intensity curve for both observers. Nonenhanced, static, and dynamic enhancement MR imaging improved differentiation between benign and malignant orbital masses in adult patients. (orig.)
[en] The production of CSF (Colony Stimulating Factor) by leukocytes of normal subjects and subjects with CML (Chronic Myeloid Leukemia) were compared, using the following technics: leukocytes separation, measurement of CSF activity. The results have shown that blood leukocyte stimulating activity of subjects with CLM is lower than in normal subjects
[fr]On a compare la production de CSF (Colony Stimulating Factor) par les leucocytes du sang peripherique de sujets normaux et de sujets atteints de LMC, a l'aide des techniques suivantes: separation des leucocytes; dosage de l'activite CSF des fractions obtenues. Les resultats ont montre que l'activite stimulante des leucocytes du sang peripherique de sujets atteints de LMC est tres inferieure a celle que l'on observe chez les sujets normaux
[en] To better understand the role of the canonical Wnt signaling pathway in cartilage development, we adenovirally expressed a constitutively active (Canada) or a dominant negative (dn) form of lymphoid enhancer factor-1 (LEF-1), the main nuclear effector of the pathway, in undifferentiated mesenchymal cells, chondrogenic cells, and primary chondrocytes, and examined the expression of markers for chondrogenic differentiation and hypertrophy. caLEF-1 and LiCl, an activator of the canonical pathway, promoted both chondrogenic differentiation and hypertrophy, whereas dnLEF-1 and the gene silencing of β-catenin suppressed LiCl-promoted effects. To investigate whether these effects were dependent on Sox9, a master regulator of cartilage development, we stimulated Sox9-deficient ES cells with the pathway. caLEF-1 and LiCl promoted both chondrogenic differentiation and hypertrophy in wild-type, but not in Sox9-deficient, cells. The response of Sox9-deficient cells was restored by the adenoviral expression of Sox9. Thus, the canonical Wnt signaling pathway promotes chondrocyte differentiation in a Sox9-dependent manner
[en] Immortalized human hepatocytes (IHH) could provide an unlimited supply of hepatocytes, but insufficient differentiation and phenotypic instability restrict their clinical application. This study aimed to determine the role of hepatocyte nuclear factor 4A (HNF4A) in hepatic differentiation of IHH, and whether encapsulation of IHH overexpressing HNF4A could improve liver function and survival in rats with acute liver failure (ALF). Primary human hepatocytes were transduced with lentivirus-mediated catalytic subunit of human telomerase reverse transcriptase (hTERT) to establish IHH. Cells were analyzed for telomerase activity, proliferative capacity, hepatocyte markers, and tumorigenicity (c-myc) expression. Hepatocyte markers, hepatocellular functions, and morphology were studied in the HNF4A-overexpressing IHH. Hepatocyte markers and karyotype analysis were completed in the primary hepatocytes using shRNA knockdown of HNF4A. Nuclear translocation of β-catenin was assessed. Rat models of ALF were treated with encapsulated IHH or HNF4A-overexpressing IHH. A HNF4A-positive IHH line was established, which was non-tumorigenic and conserved properties of primary hepatocytes. HNF4A overexpression significantly enhanced mRNA levels of genes related to hepatic differentiation in IHH. Urea levels were increased by the overexpression of HNF4A, as measured 24 h after ammonium chloride addition, similar to that of primary hepatocytes. Chromosomal abnormalities were observed in primary hepatocytes transfected with HNF4A shRNA. HNF4α overexpression could significantly promote β-catenin activation. Transplantation of HNF4A overexpressing IHH resulted in better liver function and survival of rats with ALF compared with IHH. HNF4A improved hepatic differentiation of IHH. Transplantation of HNF4A-overexpressing IHH could improve the liver function and survival in a rat model of ALF. - Highlights: • Immortalized human hepatocytes (IHH) could provide an unlimited supply of hepatocytes. • Hepatocyte nuclear factor 4A (HNF4A) plays a role in hepatic differentiation. • HNF4A improved hepatic differentiation of IHH. • Transplantation of HNF4A-overexpressing IHH could improve liver function.
[en] To determine the effects of prenatal administration of valproic acid on the developmental gross morphology of pancreas in chick embryo. Study Design: Experimental study. Place and Duration of Study: Anatomy Department, Regional Centre, College of Physicians and Surgeons, Islamabad, from February 2010 to February 2011. Methodology: An experimental group-A and control group-B, comprised of 30 eggs each. Freshly laid fertilized chicken eggs of experimental group were injected with valproic acid, incubated and hatched. Eggs of control group underwent sham treatment using normal saline. The chicks were sacrificed on hatching or day 22 of incubation, whichever was earlier. The pancreata of only alive chicks of both groups were dissected out, and evaluated for gross morphology in terms of length and weight by statistically comparing with control ones. Then pancreata were stained with aldehyde fuchsin and orange-G stain to study other obvious histological effects, if any. Results: Chicken embryos exposed to valproic acid in ovo, showed significant decrease in length and weight of pancreata. The mean of length (cm) of pancreata in group-A was 2.208 +- 0.166, and group-B was 2.300 +- 0.102 (p=0.008). The mean of weight (g) of pancreata in group-A was 0.032 +- 0.009, and group-B was 0.048 +- 0.005 (p=0.001). Conclusion: Valproic acid exposure showed retarding effect on the gross development of pancreas as depicted by decrease in the length and weight of pancreata. (author)