Search

Prostaglandin [E.sub.1] ([PGE.sub.1]) is a member of the prostaglandins and has a variety of cardiovascular protective; effects. Increasing attention has been paid to the anti-inflammation activity of [PGE.sub.1], but little direct evidence has been found. We investigated the effects of [PGE.sub.1] on cell adhesion and inflammation and the mechanisms responsible for this activity in tumor necrosis factor (TNF)-treated human umbilical vein endothelial cells. Results demonstrated that pretreatment with [PGE.sub.1] decreased the adhesion between vascular endothelial cells and monocytes, reduced the expression of vascular cell adhesion molecule-1, intercellular adhesion molecule-1, and E-selectin in vascular endothelial cells. In addition. [PGE.sub.1] suppressed TNF-induced NF-κB activation and production of reactive oxygen species. We concluded that [PGE.sub.1] suppressed the vascular inflammatory process, which might be closely related to the inhibition of reactive oxygen species and NF-κB activation in human umbilical vein endothelial cells. Key words: prostaglandin [E.sub.1], cell adhesion molecules, inflammation, NF-κB, endothelial cells. La prostaglandine [E.sub.1] ([PGE.sub.1]), qui appartient a la famille des prostaglandines, exerce une variete d'effets cardioprotecteurs. L'activite anti-inflammatoire de la [PGE.sub.1] fait l'objet d'un interet croissant, mais il existe peu de donnees probantes directes sur celle-ci. Nous avons examine les effets de la [PGE.sub.1] relativement a l'adhesion cellulaire et a l'inflammation et les mecanismes possibles responsables de cette activite dans des cellules endotheliales de la veine ombilicale humaine traitees au moyen du TNF (factor de necrosis tumorale). Les resultats ont demontre qu'un pretraitement avec la [PGE.sub.1] a diminue l'adhesion entre les cellules endotheliales et les monocytes vasculaires, et reduit l'expression de la molecule-1 d'adhesion cellulaire vasculaire, de la molecule-1 d'adhesion intercellulaire et de la selectine-1 dans les cellules endotheliales vasculaires. De plus, la [PGE.sub.1] a supprime l'activation de NF-κB induite par TNF ainsi que la production d'especes reactives de l'oxygene. Nous avons conclu que la [PGE.sub.1] a supprime le processus inflammatoire vasculaire, un effet qui pourrait etre etroitement lie a l'inhibition d'especes reactives de l'oxygene et de l'activation NF-κB dans des cellules endotheliales de la veine ombilicale humaine. Mois-cles : prostaglandine [E.sub.1], molecules d'adhesion cellulaire, inflammation, NF-κB, cellules endotheliales. [Traduit par la Redaction], Introduction Vascular endothelium is not merely a selective permeability barrier between blood and vascular smooth muscle, but actively maintains homeostasis of blood circulation (Ando and Kamiya 1993). Atherosclerosis is now [...]

Objective: Male breast cancer (BC) is a rare disease, having different clinicopathological features and survival outcomes from female patients. The aim of this research was to, combine with molecular subtypes, analyze the metastatic patterns, and prognosis between male and female patients, and to determine whether the gender was the independent prognostic factor for BC. Methods: Data used in this study were acquired from the SEER database from 2010 to 2016. The clinicopathology features and metastatic patterns were compared by the Chi‐square test and Fisher's exact test. Kaplan–Meier method was performed to compare overall survival (OS) and factors correlated with OS were determined by Cox regression models. Competing risk models were used to ascertain factors related to breast cancer‐specific death (BCSD). Results: Compared with female BC, the incidence of regional LN (HR 1.849, 95% CI 1.674–2.043, p < 0.001) and distant metastasis (HR 1.421, 95%CI: 1.157–1.744, p < 0.001) was higher in male BC. For regional LN metastasis, hormone receptor (HoR)−/HER2+ subtype occupied the majority in both male (55.56%) and female (36.86%) groups. For distant metastasis, HoR−/HER2− subtype (21.26%), and HoR−/HER2+ (7.67%) were in major in male and female group separately. Male patients shared similar combinations of metastases with female groups as for single‐site, bi‐site, and tri‐site metastasis. Gender was an independent prognostic factor for OS (p < 0.001) but not for BCSD(p = 0.620). In subgroup of patients with HoR+/HER2−(OS: p = 0.003; BCSD: p = 0.606), HoR+/HER2+(OS: p = 0.003; BCSD: p = 0.277), regional LN positive(OS: p = 0.005; BCSD: p = 0.379), or bone metastasis (OS: p = 0.030; BCSD: p = 0.862), the male cohort had poorer OS but similar BCSD with female cohort. Conclusions: Compared with female patients, male BC had different metastasis patterns and prognostic outcomes, and the affection of breast subtypes on metastasis and survivorship was also different. More attention needs to be paid for specific molecular subtype and more personalized therapeutic strategies should be customized while treating male patients. [ABSTRACT FROM AUTHOR]

What is known and objective: Suppression of antilymphoma effector cells, mainly T cells, is a key prerequisite for tumorigenesis and resistance in diffuse large B‐cell lymphoma (DLBCL). The aim of the study was to determine whether mannatide (MT), an immunomodulator, could enhance the immunological response in DLBCL patients receiving standard regimens. Methods: Patients with aggressive DLBCL treated with first‐line standard regimens were included in this single‐centre retrospective study. T‐cell subtypes were detected using flow cytometry before and after the first cycle of treatment. Patients in MT group were treated with MT combined with standard first‐line regimens, and patients in control group with standard first‐line regimens. Chi‐square test or Fisher's exact tests were used for categorical variables and independent t‐tests for continuous variables. Results and discussion: Among the 138 DLBCL patients enrolled in this study, 34 (24.64%) were assigned to the MT group, while 104 (75.36%) patients were included in the control group. There were no significant differences in clinicopathological characteristics and baseline T‐cell subtypes between the two groups (p > 0.05). After treatment, CD3+CD8+ T‐cell percentage of MT group was significantly higher than that of control group (p = 0.01), while CD3+CD4+ T‐cell percentage of MT group was significantly lower than that of control group (p < 0.01). Thus, the CD4+/CD8+ ratio of MT group was significantly lower than that of control group (p = 0.03). In the subgroup of DLBCL patients treated with EPOCH/R‐EPOCH, significant differences were also found in post‐treatment CD3+CD8+ T‐cell percentage (p < 0.01), CD3+CD4+ T‐cell percentage (p = 0.02) and CD4+/CD8+ ratio (p = 0.01) between MT and control groups. What is new and conclusion: CD3+CD8+ T‐cell percentage increased in DLBCL patients receiving MT treatment. Further studies are required to determine the clinical benefits of MT. [ABSTRACT FROM AUTHOR]

This article has been withdrawn at the request of the author(s). The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at http://www.elsevier.com/locate/withdrawalpolicy., (Copyright © 2010. Published by Elsevier Ltd.. All rights reserved.)