Histology and histopathology Vol.29, nº 2 (2014)

Ir a Estadísticas

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    Functional analysis of NPHS1 mutations in Japanese patients
    (F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2014) Miyai, Takayuki; Aya, Kunihiko; Takaiwa, Masanori; Yan, Kunimasa; Sado, Yoshikazu; Tanaka, Hiroyuki; Morishima, Tsuneo
    Background: Many mutations in the NPHS1 gene were detected among patients with congenital nephrotic syndrome. Functional analysis of those mutations was done with a stable-expression cell line. Nevertheless, establishing such a cell line is time-consuming. Methods and Results: We established an easier method using automatic counting software for functional analysis with transient-transfection cells rather than a stable-expression cell line. We demonstrated maltrafficking to the plasma membrane of abnormal nephrin for immunostaining on transient-expression cells by comparison without Triton X (detecting proteins on the cell membrane only) and with Triton X (detecting proteins both on the cell membrane and inside the cell cytoplasm). We obtained relevant results with data obtained previously using a stable-expression cell line. Furthermore, we conducted functional analysis of NPHS1 mutations in Japanese patients with congenital nephrotic syndrome using this simple method, which revealed that all pathogenic mutations impaired trafficking to the protein plasma membrane. Conclusions: Functional analysis using transient-expression cells with automatic counting software was useful to demonstrate maltrafficking to the plasma membrane of a protein. All pathogenic mutations detected in Japanese patients impaired trafficking to the protein plasma membrane.
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    Placental growth factor and soluble Fms-like tyrosine kinase 1 in diabetic pregnancy: A possible relation to distal villous immaturity
    (F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2014) El-Tarhouny, Shereen A.; Almasry, Shaima M.; Elfayomy, Amr K.; Baghdadi, Hussam; Habib, Fawzia A.
    This study aimed to describe the prevalence of chorionic distal villous immaturity (DVI) in overt diabetic/gestational diabetic (OD/GD) women compared with normoglycemic ones and to analyze the relation of DVI index (DVII) to placental growth factor (PlGF) and soluble Fms-like tyrosine kinase 1 (sFlt-1). Three groups were studied; normoglycemics (n=21), OD (n=17) and GD (n=20). Maternal blood samples were evaluated regarding serum levels of PlGF and sFlt-1. Immunohistochemical methodologies were employed in term placentae of all subjects to assess DVII and area% of PlGF and sFlt-1 immunostaining. We found that mean Hemoglobin A1c (HbA1c) is 5.22±0.15 in normoglycemics, 6.2±0.3 in OD, and 5.70±0.23 in GD with significant differences between groups (p=0.012). DVII was significantly higher in OD (66.6±4.7) and GD (72.4±4.5) compared to controls (11.6±2.5; p=0.000). Healthy women have significantly lower levels of PlGF (86.6±14.5) compared to OD (166.6±22.4, p=0.000) and GD (150.3±23.97, p=0.000) and their placentae expressed a significantly lower area% of PlGF (6.5±0.8) compared to OD (14.8±1.0, p=0.000) and GD (18.8±1.3, p=0.000). Also, normoglycemic women have significantly lower levels of sFlt-1 (108.9±12.1) compared to OD (226.5±18.6, p=0.000) or GD (197.2±16.8, p=0.000) and their placentae expressed a significantly lower area% of sFlt-1 (3.2±0.3) compared to OD (15.4±1.7, p=0.000) and GD (16.9±1.2, p=0.000). There was significant correlation between DVII and both serum level and area% of PlGF and sFlt-1 expression in the 3 groups. This study provided a new score for evaluating DVI in normal and diabetic placentae and suggested a role for PlGF and sFlt-1 in regulation of DVI in diabetic pregnancies.
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    Somatic mutation of KIT is rare in small cell lung cancer patients from Northeast China
    (F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2014) Xuan, Hong; Jingshu, Geng; Fang, Yang; Na, Li; Xiaolin, Sheng; Zhaoyang, Yang; Meng, Wang; Gongyan, Chen
    Studies have confirmed that protein overexpression or mutations of KIT are involved in growth and development of a variety of cancers. however, little is known about data of gene mutation and protein expression in small cell lung cancer (SCLC) patients from northeast China.The aim of study is to investigate gene mutation and protein expression in such patients with small cell lung cancer (SCLC) and analyse their clinical significance.The expression of c-Kit protein was analyzed by immunohistochemistry in 77 SCLC samples and 22 normal lung samples. KIT mutations were screened in exons 9, 11, 13, 14, 17 and 18 by DNA direct sequencing.The study showed that positive staining for c-Kit was observed in 28 of 77 SCLC patients . There was no correlations between expression of c-Kit and sex, ages, smoking status, stage. only 1 case was found to have known T801I mutation in exon 17. The median survival (13.9 months) of cases with c-Kit-positive was shorter than that (19.9 months)of cases with c-Kit-negative. The finding revealed that stages was identified as an independent predictive factor for SCLC patients.Our finding reveals that somatic mutation of KIT is rare in SCLC patients from the northeast China and there is no enough evidence comfirming KIT inhibitors for treatment in SCLC.
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    Retrospective study of hepatocellular adenomas based on the phenotypic classification system: A report from China
    (F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2014) Pan, Jinfeng; Chen, Lingli; Fan, Jia; Zhou, Jian; Qin, Lunxiu; Tan, Yun-Shan; Ji, Yuan; Huang, Xiaowu
    A molecular and pathological classification system for hepatocellular adenomas (HCAs) was recently introduced in Europe, resulting in four major identified subgroups. Asian countries have a considerably lower incidence of HCA as well as a different etiology. We aimed to characterize HCAs in a Chinese population based on this new classification system. A series of 30 patients with HCA were analyzed based on the phenotypic classification system using immunohistochemical analysis. Investigated antigens included liver-fatty acid binding protein (L-FABP), glutamine synthetase (GS), ß-catenin, serum amyloid A (SAA), and C-reactive protein (CRP). Of the 30 cases (20 female) included in this study, only one had a history of oral contraceptive use. We identified 9 (30%) hepatocyte nuclear factor (HNF)-1α-inactivated HCAs, 3 (10%) ß-catenin-activated HCAs, 11 (36.7%) inflammatory HCAs, and 7 (23.3%) unclassified HCAs. In the inflammatory HCA group, 2 cases demonstrated concurrent ß-catenin-activation. Homogeneous steatosis (6/9) and microadenomas (2/9) were more frequently observed in HNF1α-inactivated HCAs. A body mass index (BMI) of greater than 25 (5/11), alcohol use (4/11), and steatosis in background liver (3/11) were more frequent in inflammatory HCAs. ß-catenin-activated HCAs were larger than those of other subgroups. Despite obvious differences in etiology and gender proportion compared with Western countries, the clinical and pathological characteristics of HCA subgroups in China are similar to those in Europe. The phenotypic classification system could be reliably applied to Chinese patients as a meaningful tool for HCA management.
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    Detection of galectin-3 and localization of advanced glycation end products (AGE) in human chronic skin wounds
    (F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2014) Pepe, Daniel; Elliott, Christopher G.; Forbes, Thomas L.; Hamilton, Douglas W.
    The matricellular protein galectin-3 (Gal-3) is upregulated in excisional skin repair in rats where it has been shown to modulate the inflammatory phase of repair. Recent research into kidney pathology has implicated Gal-3 as a receptor for advanced glycation end products (AGE), resulting in the binding and clearance of these molecules. AGEs are thought to contribute to defective skin repair in diabetic patients as well as a result of the normal aging process. However, the distribution and localization of Gal-3 and AGEs has never been performed in human chronic skin wound tissue. Using immunohistochemistry, the localization of Gal-3 and AGEs in tissue isolated from chronic wounds and non-involved skin from the same patient was investigated. Of the 16 patients from which tissue was isolated, 13 had type II diabetes, one had type I diabetes and 2 patients without diabetes were also examined. In non-involved dermis, Gal-3 was detected strongly in the epidermis and in the vasculature. However, at the wound edge and in the wound bed, the level of Gal-3 labelling was greatly reduced in both the epidermis and vasculature. Labelling of serial sections for Gal-3 and AGE demonstrated that where Gal-3 immunoreactivity is reduced in the epidermis and vasculature, there is a concomitant increase in the level of AGE staining. Interestingly, similar labelling patterns were evident in diabetic and non-diabetic patients. The results from our study demonstrate an inverse correlation between Gal-3 and AGEs localization, suggesting that Gal-3 may protect against accumulation of AGEs in wound healing.