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A. P. Dei Tos Paola Dal Cin 《Virchows Archiv : an international journal of pathology》1997,431(2):83-94
Soft tissue tumours represent a heterogeneous group of mesenchymal lesions, and their classification is the subject of continuous
debate. Chromosome analysis, molecular cytogenetics and molecular assays may become increasingly useful in diagnosis, and
this review summarises advances in the cytogenetic characterisation and classification of soft tissue tumours. Among the group
of fibrous lesions, superficial fibromatosis exhibits trisomy 8. This genomic change is also observed in desmoid fibromatosis
in association with trisomy 20. Trisomy 11 is the most frequently observed chromosomal aberration in congenital fibrosarcoma.
Dermatofibrosarcoma protuberans and giant cell fibroblastoma share a translocation t(17;22), which supports the concept of
the existence of a common differentiation pathway. Adipose tissue tumours is the group in which integration of genetics and
pathology has been most fruitful. Ordinary lipomas cytogenetically show an abnormal karyotype in about half the cases. Genomic
changes of the 11q13 region are observed in hibernoma. Lipoblastoma exhibits a specific 8q rearrangement in 8q11-q13. Loss
of material from the region 16q13-qter and 13q deletions are observed in spindle cell/pleomorphic lipomas. The well-differentiated
liposarcoma/atypical lipoma group is characterised karyotypically by the presence of one extra ring and/or extra giant chromosome
marker. Myxoid and round cell liposarcoma share the same characteristic chromosome change: t(12;16)(q13;p11) in most cases.
In the group of smooth muscle lesions most data are derived from uterine leiomyomas, which can be subclassified cytogenetically
into seven different types. Half of all leiomyomas are chromosomally normal; the other half have one of six possible consistent
chromosome changes. Alveolar rhabdomyosarcoma is characterised cytogenetically by two variant translocations t(2;13)(q35;q14)
and t(1;13)(p36;q14). Among tenosynovial tumours, the localised type of giant cell tumour of tendon sheath exhibits two different
karyotypic changes. One involves 1p11 in a translocation with chromosome 2 or with another chromosome. A second type involves
16q24. Synovial sarcoma is characterised cytogenetically by a translocation occurring between chromosome 18 and presumably
two adjacent loci on the X chromosome. In neural tumours, abnormalities of chromosome 22 have been reported in benign schwannomas
and perineuriomas. Malignant peripheral nerve sheath tumours exist in two main forms: sporadic and associated with the NF-1
syndrome. Karyotypes are very complex, but chromosomes 17q and 22q are very often involved. Clear cell sarcoma is characterised
cytogenetically and molecularly by a translocation t(12;22)(q13;q12). The Ewing’s sarcoma/peripheral neuroectodermal tumour
category shows a central karyotypic anomaly represented by the translocation t(11;22). The two variants t(21;22) and t(7;22)
are found in some cases. Among cartilaginous lesion, the most frequently described anomaly is the t(9;22)(q22;q12) in extraskeletal
myxoid chondrosarcoma. Intra-abdominal desmoplastic small round cell tumour is characterised by a t(11;22)(p13;q12).
Received: 5 February 1997 / Accepted: 24 February 1997 相似文献
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B Albertino G Gasparri P A Casalegno A Oliaro M Dei Poli 《Minerva chirurgica》1990,45(15-16):997-1002
The paper reports the epidemiology and causal factors of esophageal carcinoma, and compares the authors' personal experience with already published data. The clinical importance of epidemiology is stressed as a means of identifying risk factors for esophageal carcinoma, thus aiding an early diagnosis. The authors underline the central role of surgery in the treatment of esophageal carcinoma. 相似文献
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实验性局灶性脑缺血再灌注Fos蛋白的表达 总被引:1,自引:0,他引:1
目的 探讨大鼠局灶性脑缺血再灌注Fos蛋白表达的意义及其机制。方法 采用免疫组化法观察Fos蛋白在大鼠局灶性脑缺血再灌注后皮层和基底节区的动态变化。结果 Fos蛋白在大脑中动脉阻断 1h后 ,随再灌注时间延长其分布不同。基底节区持续时间长 ,阳性细胞多 ,而皮层持续时间短 ,阳性细胞少。其中再灌注 90min ,Fos蛋白表达最显著。大脑中动脉供血中心区皮层几无表达。结论 Fos蛋白的表达与神经细胞存活密切相关 ,出现Fos蛋白表达的区域神经元易于耐受缺血性损害而存活 ,可能是神经细胞自我保护机制之一 ,Fos蛋白的表达存在扩散抑制 相似文献
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Giulia Franzoni Susanna Zinellu Elisabetta Razzuoli Lorena Mura Chiara G. De Ciucis Livia De Paolis Tania Carta Antonio G. Anfossi Simon P. Graham Bernardo Chessa Silvia Dei Giudici Annalisa Oggiano 《Viruses》2022,14(10)
Toll-like receptor 2 (TLR2) ligands are attracting attention as prophylactic and immunopotentiator agents against pathogens, including viruses. We previously reported that a synthetic diacylated lipopeptide (Mag-Pam2Cys_P48) polarized porcine macrophages towards a proinflammatory antimicrobial phenotype. Here, we investigated its role in modulating monocyte-derived macrophage (moMΦ) responses against African swine fever virus (ASFV), the etiological agent of one of the greatest threats to the global pig industry. Two ASFV isolates were compared: the attenuated NH/P68 and the virulent 26544/OG10. No effect on virus infection nor the modulation of surface markers’ expression (MHC I, MHC II DR, CD14, CD16, and CD163) were observed when Mag-Pam2Cys_P48 treated moMΦ were infected using a multiplicity of infection (MOI) of 1. Mag-Pam2Cys_P48 treated moMΦ released higher levels of IL-1α, IL-1β, IL-1Ra, and IL-18 in response to infection with NH/P68 ASFV compared to 26544/OG10-infected and mock-infected controls. Surprisingly, when infected using a MOI of 0.01, the virulent ASFV 26544/OG10 isolate replicated even slightly more efficiently in Mag-Pam2Cys_P48 treated moMΦ. These effects also extended to the treatment of moMΦ with two other lipopeptides: Mag-Pam2Cys_P80 and Mag-Pam2Cys_Mag1000. Our data suggested limited applicability of TLR2 agonists as prophylactic or immunopotentiator agents against virulent ASFV but highlighted the ability of the virulent 26544/OG10 to impair macrophage defenses. 相似文献
9.
Heart failure (HF) affects approximately 1–2?% of the adult population. Diabetes mellitus (DM) is one of the most frequent comorbidities in HF, portending a worse prognosis. DM is associated with an increased risk of artery disease, and consequently of post-ischemic HF, but it may also alter directly the myocardial structure and function. Insights into the pathophysiological mechanisms of diabetic cardiomyopathy have been provided by both experimental and clinical investigations. In recent years, it has emerged that the fibrotic process is a result of the convergence of multiple neurohormonal alterations in diabetic cardiomyopathy at the basis of disease progression and phenotype determination: HF with reduced or preserved ejection fraction. Therapies for HF and DM should demonstrate an improved prognosis and have a neutral effect on glucose homeostasis and the risk of HF development. 相似文献
10.
D'Aloia A Faggiano P Fiorina C Vizzardi E Bontempi L Grazioli L Dei Cas L 《International journal of cardiology》2003,90(2-3):327-329
Congenital anomalies of the inferior vena cava such as absence or atresia are uncommon vascular defects and result from aberrant development during embryogenesis. We report a case of a young female patient affected by proximal deep venous thrombosis (DVT) complicated by liver and pulmonary embolism; subsequent extensive evaluation revealed the congenital absence of infrarenal inferior vena cava, with emboli probably occurring through collateral veins. Accordingly, in young patients with idiopathic DVT of the lower extremities and pelvic veins, the presence of inferior vena cava abnormalities should always be considered and investigated, together with classic coagulation factors, as a factor predisposing to thromboembolic complications. 相似文献