Histology and histopathology Vol.25, nº4 (2010)

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http://hdl.handle.net/10201/177541

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Open Access
Absorptive activities of the efferent ducts evaluated by the immunolocalization of aquaporin water channels and lectin histochemistry in adult cats
(Murcia: F. Hernández, 2010) Arrighi, S.; Ventriglia, G.; Aralla, M.; Zizza, S.; Di Summa, A.; Desantis, S.
Ultrastructural and biochemical features of efferent ducts (EDs) are indicative of an intense absorptive activity towards the luminal fluid. This function was investigated by 1) the immunohistochemical localization of different aquaporins, integral membrane water channels that facilitate rapid passive movement of water, and 2) the histochemical localization of lectins, known to have specific affinity for glycoconjugate residues. AQP1 was mostly revealed at the apical surface and adluminal cytoplasm of non-ciliated cells and to a minor extent in their lateral plasma membrane, whereas it was absent in ciliated cells. Blood vessels showed AQP1-immunoreactivity, which was present in endothelial cells of venous vessels and capillaries and around the muscular sheath of arteries. AQP9 was expressed in the apical zone of ciliated and non-ciliated cells and in the lateral cell membrane. AQP2 and AQP5 were undetectable. Lectin histochemistry showed that non-ciliated cells contain glycans with terminal Neu5Acα2,3Galß1,3GalNAc, Neu5Acα2,3Galß1,4GlcNAc, Galß1,4GlcNAc, GalNAc (s-PNA, MAL II, RCA120, SBA reactivity) and with internal/terminal αMan (Con A affinity) at the luminal surface and the apical region. In addition, non-ciliated cells expressed oligosaccharides terminating with GalNAc and Neu5Acα2,6Gal/GalNAc (SNA reactivity) in the luminal surface and the apical zone, respectively. Ciliated cells revealed glycoconjugates only on cilia, which showed terminal Neu5Acα2,3Galß1,4GlcNAc (s-RCA120 staining) and GalNAc, as well as internal/terminal αMan and GlcNAc (s-WGA, GSA II staining). Data provide evidence for the involvement of different pathways in the bulk reabsorption of water and low molecular weight solutes by the non-ciliated cell of the cat EDs. AQP-mediated trans-cellular route can be hypothesized, together with fluid phase endocytosis mediated by the glycocalix and a well-developed endocytotic apparatus. Epithelial ciliated cells, whose main function is the movement of luminal content, might also participate in absorptive processes to a lesser extent
Open Access
The pathobiological behaviors and prognosis associated with Japanese gastric adenocarcinomas of pure WHO histological subtypes
(Murcia : F. Hernández, 2010) Zheng, Hua-Chuan; Zheng, Yu-shuang; Xia, Pu; Xu, Xiao-yan; Xing, Ya-nan; Takahashi, Hiroyuki; Guan, Yi-Fu; Takano, Yasuo
Japan is a high-risk region for gastric carcinoma with a comparatively early stage and favorable prognosis. To clarify the pathobiological behaviors and prognosis of Japanese gastric adenocarcinoma, we analyzed the clinicopathological characteristics of different WHO subtypes of carcinomas. The expression of ki-67, CPP32, p53, FHIT, maspin, parafibromin, GRP78, GRP94, EMMPRIN, VEGF, P-GSK3ß-ser9, fascin, cortactin, Arp2, Arp3 MUC-2, MUC-5AC and MUC-6 was examined using immunohistochemistry and tissue microarrays. The majority of cases were well-, poorly-, or moderatelydifferentiated subtype, whereas the minority were papillary or signet ring cell carcinoma (SRC). Patients with poorly-differentiated or SRC carcinoma were predominantly young and female. Poorly-differentiated and mucinous carcinomas were larger, with deeper invasion, more venous or lymphatic invasion, frequent lymph node involvement and peritoneal dissemination, or higher staging. The SRC group exhibited weaker expression of ki-67, CPP32, p53, parafibromin, GRP78, GRP94, P-GSK3ß-ser9, VEGF or cortactin. The moderately-differentiated subtype exhibited lower expression of FHIT and Arp3 positivity. The poorlydifferentiated group showed weaker expression of CPP32, EMMPRIN, MUC-2, MUC-5AC, and MUC-6. Survival analysis indicated that the patients with poorlydifferentiated or mucinous subtypes had a lower cumulative survival rate than those with papillary, well-, moderately-differentiated, or SRC carcinomas (P<0.05). The age, invasive depth, lymphatic invasion, peritoneal dissemination, and WHO classification were independent prognostic factors for carcinoma patients (P<0.05). It was suggested that poorly-differentiated and mucinous subtypes are more aggressive and of unfavorable prognosis among Japanese gastric carcinomas. Lower levels of proliferation and apoptosis, as well as alterations in tumor suppressor genes, mucin production and ER stress protein played important roles in the pathogenesis of poorly-differentiated and SRC carcinomas.
Open Access
Non-compaction of the ventricular myocardium, a cardiomyopathy in search of a pathoanatomical definition
(Murcia : F. Hernández, 2010) Val-Bernal, José Fernando; Garijo, M.F.; Rodriguez-Villar, Diana; Val, D.
Ventricular non-compaction is a rare cardiomyopathy characterized by numerous, excessively prominent ventricular trabeculations and deep intertrabecular recesses communicating with the ventricular cavity. The lesion is postulated to result from an intrauterine developmental arrest that stops compaction of the myocardial fiber meshwork. This cardiomyopathy affects the left ventricle, with or without concomitant right ventricular involvement. The disease is now seen with increasing frequency and it is clinically diagnosed by imaging techniques such as echocardiography or cardiac magnetic resonance. Current diagnostic criteria are considered too sensitive, particularly in black individuals. Therefore, this condition has generated considerable controversy and demands a new definition. Non-compaction cardiomyopathy shows variability of hereditary patterns, genetic heterogeneity, diversity in associated phenotypes and a wide spectrum of clinical presentation and pathophysiological findings. Non-compaction can be simply a variant of normal maturation of the ventricular myocardium with only the most severe forms producing a distinct clinical-pathological entity. Ventricular noncompaction most probably is a secondary consequence of an underlying molecular derangement produced by a pathogenetic mutation. It is likely that surgical pathologists will find this entity more frequently due to involvement in transplantation teams.
Open Access
TGF-B1 and VEGF after fresh frozen bone allograft insertion in oral-maxillo-facial surgery
(Murcia : F. Hernández, 2010) Rodella, L.F.; Favero, G.; Boninsegna, R.; Borgonovo, A.; Rezzani, R.; Santoro, F.
Bone regeneration technique using allografts is widely used in oral surgery to repair alveolar defects and to increase alveolar volume for endosseous implant insertions. Bone allografts promote the reabsorption and neo-synthesis of bone tissue, which are regulated by numerous cytokines, proteins and growth factors. In this study, six patients with insufficient alveolar volume for endosseous implant insertions, were treated with bone regeneration technique using Fresh Frozen Bone (FFB) allografts collected from the femoral head or the hip. Samples of bone graft collected during graft insertion surgery and biopsies collected six months later during implantology were fixed, decalcified and analyzed histomorphologically and morphometrically by haematoxylin-eosin staining. In addition, TGF-ß1 and VEGF were analyzed by immunohistochemistry. The histological analysis of FFBs showed wide areas of calcified bone organized in osteons intermingled with areas of non-calcified matrix containing osteoblasts. However, the regenerated alveolar bone, collected six months after the graft insertion surgery, showed wide areas of non-calcified matrix. TGF-ß1 and VEGF were less expressed in FFB than in regenerated alveolar bone
Open Access
Tumor suppression by p53, making cells senescent
(Murcia : F. Hernández, 2010) Qian, Yingjuan; Chen, X.
Cellular senescence is a permanent cell cycle arrest and a potent tumor suppression mechanism. The p53 tumor suppressor is a sequence-specific transcription factor and acts as a central hub sensing various stress signals and activating an array of target genes to induce cell cycle arrest, apoptosis, and senescence. Recent reports showed that restoration of p53 induces premature senescence and tumor regression in mice with hepatocarcinomas or sarcomas. Thus, p53- mediated senescence is capable of eliminating cancer cells in vivo. p63 and p73, two homologues of p53, have similar function in cell cycle arrest and apoptosis. However, the role of p63 and p73 in cellular senescence is elusive. In this review, we will discuss how p53 regulates senescence and future studies about p53 family members in senescence.

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