BackgroundThe purpose of this study was to (1) identify specific miRNAs in growth hormones (GH)-secreting pituitary adenomas; (2) determine the relationship between the expression of these miRNAs and tumor size, somatostatin analogs treatment, and responsiveness to somatostatin analogs (SSA).MethodsFifteen GH-secreting adenomas patients were treated with lanreotide for 4 months before surgery. Patients with 50% reduction of GH secretion by lanreotide were considered as SSA responders, while patients with less than 50% of GH reduction were considered as SSA nonresponders. We analyzed the miRNAs in 21 GH-secreting pituitary adenomas and 6 normal pituitaries by miRCURY™ LNA array and some differentially expressed miRNAs were validated by quantitative real-time PCR.ResultsFifty-two miRNAs were differentially expressed between GH-secreting pituitary adenomas and normal pituitaries. Differential expression of 9 miRNAs was observed between micro- and macro-adenomas. Thirteen miRNAs were differentially expressed between tumor samples from lanreotide-treated patients and those from lanreotide-untreated patients. Seven miRNAs were differentially expressed between SSA responders or GH nonresponders. Several identified miRNAs may be involved in cell proliferation, apoptosis, cancer development and progression.ConclusionsOur results indicate that altered miRNAs expression is involved in GH-secreting pituitary adenomas transformation, which will shed light on the mechanisms for the treatment of acromegaly by SSA. Identification and characterization of the targets of altered miRNAs genes may elucidate molecular mechanisms involved in the pathogenesis of pituitary adenoma.

Objective: To investigate whether 4-month preoperative lanreotide treatment would improve the surgical cure rate of newly diagnosed acromegalic patients with macroadenomas. Design: A prospective, randomised study. Methods: After a baseline evaluation, patients were randomly assigned to 4-month preoperative treatment with lanreotide (starting with 30 mg/2 weeks i.m. and increasing to 30 mg/week i.m. at week 8 if mean GH O2.5 mg/l on GH day curves; pretreatment group, Group 1) or to transsphenoidal surgery (direct surgery group, Group 2). Cure was evaluated 4 months postoperatively primarily by fasting IGF1 less than or equal to age-adjusted upper limit of normal. Results: A pool of 108 patients was randomly divided into two groups. Five patients in each group were lost to follow-up during the study period, so 49 patients in each group were analysed. At baseline, no difference was observed between the two groups. Cure was established in 24 of 49 (49.0%, 95% confidence interval (CI), 35.0-63.0%) pretreated patients (Group 1) versus 9 of 49 (18.4%, 95% CI, 7.6-29.

Servitization has been viewed as an important method for manufacturers to gain competitive advantages. The purpose of the study is to empirically examine the effects of lean and agile practices as well as mass customization and product innovation capabilities on the implementation of servitization. The hypotheses are empirically examined using structural equation modeling with data collected from 647 manufacturers. The results show that product innovation capability directly improves servitization. Although the direct effect of mass customization capability on servitization is not significant, it improves servitization indirectly through product innovation capability. The findings also reveal that the direct impacts of lean and agile practices on servitization are not significant. Lean and agile practices affect servitization indirectly through product innovation capability, whereas the indirect effects of lean and agile practices on servitization through mass customization capability are not significant. Therefore, this study draws the conclusions that a manufacturer should develop mass customization and product innovation capabilities simultaneously when implementing servitization. Moreover, a manufacturer should also invest on lean and agile practices and product innovation capability at the same time when transforming to a service-based business model to cultivate their synergies on servitization.

PET/CT may be useful to detect tumors in patients with equivocal MRI results. C-MET PET/CT can provide valuable diagnostic information when F-FDG PET/CT yields negative results, especially in patients with recurrent microadenomas.

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Our results suggest that SZ-685C induces MMQ cell apoptosis in a miR-200c-dependent manner. Therefore, SZ-685C might be a useful alternative treatment for pituitary adenoma.

Hyperprolactinemia is associated with endothelial dysfunction and atherogenic risk factors, but carotid intima media thickness (IMT) has not been studied in hyperprolactinemic patients. To determine whether untreated hyperprolactinemia contributes to increased carotid IMT. Thirty-one prolactinoma patients and 60 healthy controls were respectively studied. Participants underwent hormone evaluation. Anthropometric parameters (body mass index and blood pressure), inflammatory markers (high-sensitivity C-reactive protein and fibrinogen), serum glucose, insulin, lipid and apolipoprotein profiles were also determined. Endothelial function measured as the flow-mediated dilation (FMD) of a brachial artery and carotid IMT were evaluated using high-resolution ultrasonography. Multivariate linear regression analysis was applied to identify independent determinants of FMD and carotid IMT. Triglycerides, homeostasis model assessment of insulin resistance, apolipoprotein (apo)B/apoA-I ratio, high-sensitivity C-reactive protein (hsCRP) and fibrinogen were significantly higher, while apoA-I was significantly lower in patients with prolactinomas than in the controls. Meanwhile, decreased FMD and increased carotid IMT were observed in hyperprolactinemic group. Serum prolactin was positively correlated with triglycerides, apoB/apoA-I ratio, hypogonadal, hsCRP and fibrinogen (P < 0.05), but inversely associated with apoA-I and HDL-C (P ≤ 0.001). Moreover, prolactin was found negatively correlated with FMD (r = -0.576, P < 0.0001), and positively correlated with mean carotid IMT (r = 0.652, P < 0.0001). Multivariate regression analysis revealed that prolactin determined, independent of traditional risk factors, FMD (B = -0.589, 95% confidence interval (CI) -2.525 to -0.804, P = 0.001) and mean carotid IMT (B = 0.527, 95% CI 0.027-0.069, P < 0.0001). Hyperprolactinemia may be involved in the preclinical increase in carotid IMT, directly or by promoting atherogenic factors, including insulin resistance, low-grade inflammation and endothelial dysfunction. Additional studies are warranted to confirm our findings and explore the mechanisms underlying prolactin-associated early atherosclerosis.