Stronger Expression (stronger + expression)

Distribution by Scientific Domains


Selected Abstracts


Immunohistochemical analysis of Th1/Th2 cytokine profiles and androgen receptor expression in the pathogenesis of nifedipine-induced gingival overgrowth

JOURNAL OF PERIODONTAL RESEARCH, Issue 4 2003
W-T. Huang
Background:, Numerous studies have demonstrated that gingival overgrowth may be associated with androgen and cytokine expression in tissues. Objectives:, The aim of this study was to compare the expression of androgen receptor-presenting cells (AR+ cells) and Th1/Th2 cytokine [Th1: interleukin (IL)-2, interferon-, (IFN-,); Th2: IL-4, IL-10, IL-13] expression cells in tissue sections of patients with gingival overgrowth. Materials and methods:, Tissue samples were collected from patients with healthy periodontium (H group), adult periodontitis (P group), surgically extracted teeth (S group), and nifedipine-induced gingival overgrowth (NIGO group). The clinical periodontal parameters of pocket depth (PD), bleeding on probing (BOP), and plaque control record (PCR) were measured around selected sample teeth. Gingival biopsies were further processed by immunohistochemical staining method. The expressions of cells positive for AR, IL-2, IFN-,, IL-4, IL-10, and IL-13 were counted by predetermined semiquantitative methods. Results:, Our results indicated that AR, IL-2, IFN-,, IL-4, IL-10, and IL-13 were intensively expressed in the nuclei of inflammatory cells and fibroblasts of gingival connective tissue. Stronger expressions of AR, IL-2, and IFN-, were found in the NIGO group. The AR+ cells/0.01 mm2 in gingival fibroblasts were significantly higher in the NIGO group (80.2 ± 10.7) than those of the periodontitis group (52.5 ± 11.8) and control group (37.4 ± 11.3) (P < 0.05). The cytokine expression of the NIGO group showed a trend towards Th1-type expression (IL-2; P = 0.0001). In the surgically extracted tooth group, a stronger expression of Th2-type cytokine (IL-4, Il-10, IL-13; P < 0.05) was found in inflammatory cells. In a comparison of the IL-2/IL-4-labeled cell ratio of the four groups, a descending sequence was discovered as NIGO group (0.92 ± 0.97) > H group (0.81 ± 0.61) > P group (0.77 ± 0.82) > S group (0.58 ± 1.77). Conclusions:, Our data support the following: (i) taking nifedipine may elevate the expression of AR in susceptible oral tissue, e.g. gingiva; (ii) the cytokine profile of T-cells in NIGO tissue indicates a trend preferentially towards Th1 activity; and (iii) elevation of AR expression cells and prominent Th1 cytokine-labeled cells are two significant factors in the pathogenesis of NIGO. [source]


Peer substance involvement modifies genetic influences on regular substance involvement in young women

ADDICTION, Issue 10 2010
Arpana Agrawal
ABSTRACT Aims Peer substance involvement (PSI) is a robust correlate of adolescent substance use. A small number of genetically informative studies suggest that shared genetic and environmental factors contribute to this association. We examine mechanisms by which PSI influences the etiology of regular substance involvement (RSI), particularly in women. Design Population-based cohort study of twin women from the US Midwest. Participants 2176 twin women. Measurements To examine the relationship between self-reported PSI during adolescence and a composite RSI representing regular tobacco, alcohol and cannabis use during young adulthood, using genetically informative correlation, moderation and joint correlation-moderation models. Findings There was evidence for a significant additive genetic X environment interaction. PSI was moderately heritable (h2 = 0.25). Genetic, shared and non-shared influences on RSI overlapped with influences on PSI (genetic correlation of 0.43). Even after controlling for these shared genetic influences, RSI was more heritable in those reporting greater PSI. Conclusions While young women may select peers based on certain dispositional traits (e.g. permissiveness towards substance use), the social milieu constructed by PSI does modify the architecture of increased RSI in those individuals with increasing levels of PSI being associated with stronger expression of heritable influences. [source]


Expression of c-MET, low-molecular-weight cytokeratin, matrix metalloproteinases-1 and -2 in spinal chordoma

HISTOPATHOLOGY, Issue 5 2009
Takahiko Naka
Aims:, In skull base chordoma, c-MET expression has been reported to correlate with younger patient age and favourable prognosis; however, it also contributes to tumour invasiveness, especially in recurrent lesions, suggesting variable roles for c-MET according to clinical status. The aim of this study was to investigate the significance of c-MET expression in spinal chordoma, which affects patients who are 10,20 years older than those with skull base chordoma. Methods and results:, Using immunohistochemical techniques, the expression of c-MET and its ligand, hepatocyte growth factor (HGF) was investigated in 34 primary spinal chordomas and compared with other clinicopathological parameters. Expression of c-MET and HGF was observed in 85.3 and 21.7% of lesions, respectively. c-MET expression correlated with the expression of an epithelial marker, low-molecular-weight cytokeratin (CAM5.2). Lesions with higher c-MET expression showed significantly stronger expression of proteinases, including matrix metalloproteinase (MMP)-1 and MMP-2. However, c-MET expression was not associated with patient age, proliferative ability estimated by MIB-1 labelling index, or prognosis. Conclusions:, c-MET expression was observed in most spinal chordomas and correlated with the expression of CAM5.2, suggesting a relationship to an epithelial phenotype. [source]


Immunohistochemical analysis of Th1/Th2 cytokine profiles and androgen receptor expression in the pathogenesis of nifedipine-induced gingival overgrowth

JOURNAL OF PERIODONTAL RESEARCH, Issue 4 2003
W-T. Huang
Background:, Numerous studies have demonstrated that gingival overgrowth may be associated with androgen and cytokine expression in tissues. Objectives:, The aim of this study was to compare the expression of androgen receptor-presenting cells (AR+ cells) and Th1/Th2 cytokine [Th1: interleukin (IL)-2, interferon-, (IFN-,); Th2: IL-4, IL-10, IL-13] expression cells in tissue sections of patients with gingival overgrowth. Materials and methods:, Tissue samples were collected from patients with healthy periodontium (H group), adult periodontitis (P group), surgically extracted teeth (S group), and nifedipine-induced gingival overgrowth (NIGO group). The clinical periodontal parameters of pocket depth (PD), bleeding on probing (BOP), and plaque control record (PCR) were measured around selected sample teeth. Gingival biopsies were further processed by immunohistochemical staining method. The expressions of cells positive for AR, IL-2, IFN-,, IL-4, IL-10, and IL-13 were counted by predetermined semiquantitative methods. Results:, Our results indicated that AR, IL-2, IFN-,, IL-4, IL-10, and IL-13 were intensively expressed in the nuclei of inflammatory cells and fibroblasts of gingival connective tissue. Stronger expressions of AR, IL-2, and IFN-, were found in the NIGO group. The AR+ cells/0.01 mm2 in gingival fibroblasts were significantly higher in the NIGO group (80.2 ± 10.7) than those of the periodontitis group (52.5 ± 11.8) and control group (37.4 ± 11.3) (P < 0.05). The cytokine expression of the NIGO group showed a trend towards Th1-type expression (IL-2; P = 0.0001). In the surgically extracted tooth group, a stronger expression of Th2-type cytokine (IL-4, Il-10, IL-13; P < 0.05) was found in inflammatory cells. In a comparison of the IL-2/IL-4-labeled cell ratio of the four groups, a descending sequence was discovered as NIGO group (0.92 ± 0.97) > H group (0.81 ± 0.61) > P group (0.77 ± 0.82) > S group (0.58 ± 1.77). Conclusions:, Our data support the following: (i) taking nifedipine may elevate the expression of AR in susceptible oral tissue, e.g. gingiva; (ii) the cytokine profile of T-cells in NIGO tissue indicates a trend preferentially towards Th1 activity; and (iii) elevation of AR expression cells and prominent Th1 cytokine-labeled cells are two significant factors in the pathogenesis of NIGO. [source]