No abstract

Micro-inflammation state in T2DM was characterized by increased sIL-2 R, elevated CD3(+)CD4(+)T cells and the imbalance of Treg cells and Teff cells, which as one of the pathogeneses took part in inflammation reaction in T2DM.

Background:The clinical value of perineural invasion (PNI) in patients with localized prostate cancer (PCa) is widely explored. However, its role in metastatic PCa (mPCa) remains unknown. Objectives: We aim to investigate the clinical significance of PNI in patients with mPCa. Materials and methods: Data of 515 mPCa patients between 2012 and 2018 were retrospectively studied. PNI and its intensity were identified by prostate biopsy. The prognostic value of PNI was evaluated by Kaplan-Meier curves and Cox proportional-hazards model. Results: Perineural invasion was detected in 170/515 (33.0%) cases. Among them 73/170 (42.9%) and 97/170 (57.1%) harbored unifocal PNI (uni-PNI) and multifocal PNI (multi-PNI), respectively. Compared to patients without PNI, those with PNI had statistically shorter castration-resistant PCa-free survival (CFS) and numerically shorter overall survival (OS) (mCFS: 15.4-vs. 18.5-Mo, p = 0.015; mOS: 63.8-vs. 71.4-Mo, p = 0.108). Patients harboring multi-PNI were associated with poorer clinical outcomes than those with uni-PNI (mCFS: 12.4-vs. 18.0-Mo, p = 0.040; mOS: 39.7-Mo vs. NR, p = 0.018) or those without PNI (mCFS: 12.4-vs. 18.5-Mo, p = 0.002; mOS: 39.7-vs. 71.4-Mo, p = 0.002). Totally, neither uni-PNI nor multi-PNI was an independent risk factor impacting survival outcomes in multivariate analyses. While remarkably, for patients with favorable/intermediate-risk mPCa, multi-PNI was an independent adverse prognosticator for both CFS and OS (CFS: HR: 1.705, 95% CI: 1.029-2.825, p = 0.038; OS: HR: 3.294, 95% CI: 1.464-7.413, p = 0.004). Discussion and Conclusion: This study filled the blank of the clinical significance of PNI in mPCa. We found that multi-PNI could distinguish men with relatively poor prognosis from patients initially regarded as with favorable survival outcomes by other prognosticators, and thus, avoid disease underestimation in this group of patients. Our finding would help physicians have a deeper understanding of the heterogeneity of mPCa and make better individualized therapeutic strategy.

ABSTRACT. We aimed to determine the significance and changes in leptin, adiponectin (ADP), and visfatin levels in adults with growth hormone deficiency (GHD). Forty adults (19 men, 21 women) who had been diagnosed with GHD comprised the observation group, while 36 healthy adults (18 men, 18 women) were used as the control group. Fasting venous blood was collected to detect leptin, ADP, and visfatin levels. There was no statistically significant difference (P > 0.05) between the GHD group and the control group in terms of gender ratio, age, and body mass index. The waist-to-hip ratio (0.894 ± 0.061 vs 0.830 ± 0.481), cholesterol (4.99 ± 1.046 vs 4.18 ± 0.683), triglyceride (1.97 ± 1.428 vs 1.08 ± 0.403), LDL (2.91 ± 0.980 vs 2.29 ± 0.540), leptin (3.00 ± 1.233 vs 1.89 ± 1.554), ADP (15.26 ± 6.449 vs 10.24 ± 7.608), and visfatin levels (10.42 ± 3.715 vs 5.87 ± 3.90) in the GHD group were significantly higher than those in the control 4051 GHD and leptin, adiponectin, and visfatin ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 13 (2): 4050-4056 (2014) group (all P < 0.05). The levels of growth hormone (1.68 ± 1.67 vs 15.53 ± 6.23), insulin-like growth factor-1 (IGF-1, 22.64 ± 16.41 vs 61.85 ± 28.48), IGF-binding protein-3 (4889 ± 2962 vs 6866 ± 3823), and dehydroepiandrosterone sulfate (1.466 ± 1.804 vs 6.000 ± 2.767) in the GHD group were significantly lower than those in the control group (all P < 0.05). Correlation analysis demonstrated that leptin level was positively correlated to ADP and visfatin in both the GHD and control groups and negatively correlated to IGF-1 (r = 0.332, P < 0.05). Logistic regression analysis demonstrated that leptin, ADP, and visfatin were independent risk factors for adults with GHD.

Linked Article: Reich et al. Br J Dermatol 2017; 177:1014–1023.