Insulin-like growth factor (IgF)-I,IgF binding protein-3, and prostate cancer: correlation with gleason score

Introduction

Non-androgenic growth factors are involved in the growth regulation of prostate cancer (PCa).

Objective

This is the first Brazilian study to correlate, in a population of patients operated for PCa, PSA, total testosterone, insulin-like growth factor-I (IGF-I) and insulin-like growth factor-binding protein-3 (IGFBP-3) with Gleason score and to compare with a control group with benign prostate hyperplasia (BPH).

Materials and Methods

This retrospective single-center study included 49 men with previously diagnosed PCa and 45 with previously diagnosed BPH. PSA, testosterone, IGF-I, IGFBP-3 were determined in both groups.

Results

PSA and IGFBP-3 levels were significantly higher in the PCa group as compared to the BPH group (p<0.001 and p=0.004, respectively). There was a significant difference when we compared the PSA before surgery (p<0.001) and at the inclusion in the study (p<0.001) and IGFBP3 (0.016) among patients with Gleason <7, ≥7 and BPH. In the PCa group, PSA, testosterone, IGF-I and IGFBP-3 levels were comparable between Gleason <7 and ≥7.

Conclusions

Our data suggest that in localized PCa, the quantification of PSA and, not of IGF-1, may provide independent significant information in the aggressiveness. IGFBP-3 could be a biochemical marker of disease control in PCa patients.     

Primary cardiac angiosarcoma. A therapeutical dilemma

Cardiac angiosarcomas are malignant tumors that almost invariably have a short and fatal evolution. The therapeutic approach includes surgery, chemotherapy, and radiation therapy, alone or in combination. Heart transplantation is an attractive option in nonresectable tumors, even though the current experience is still limited. However, in most patients, the diagnosis is still established late, and survival is only slightly altered by the proposed treatments, mainly due to previously existing and undetected metastases. We report a case that illustrates the therapeutic dilemma faced with this neoplasia, and we discuss the case based on a literature review.     

Reliability and reproducibility of the method of assessment of midpalatal suture maturation: A tomographic study

Objectives:To assess reliability and reproducibility of the individual assessment of midpalatal suture maturation in computed tomography among orthodontists and radiologists for potential diagnosis application.Materials and Methods:Sixty axial slices from cone-beam computed tomography and multi-slice CT scans of patients aged between 11 and 21 years old (33 females and 27 males) were selected. For the investigation of reliability and reproducibility of the method, two groups of examiners were established. The first group consisted of 11 orthodontists and the second consisted of 10 radiologists. Each group examined the images and performed individual assessment of the midpalatal suture maturation method twice within an interval of 21 days. During the first and second analyses, the sequence of images was randomized to reduce potential bias. Weighted Cohen''s kappa was performed to assess inter- and intra-examiners'' agreement. The percentage of perfect agreement and the number of stages apart for each disagreement were calculated. The significance level was P < .05.Results:The overall inter-examiner agreement was satisfactory in the first (kappa_w: 0.37) and the second (kappa_w: 0.34) analyses. Intra-examiner agreement outcomes were similar between orthodontists (kappa_w: 0.44) and radiologists (kappa_w: 0.41). The percentage of perfect agreement was 43.2%.Conclusions:The method for individual assessment of midpalatal suture maturation revealed potential reliability and reproducibility. However, the agreement rate observed in the present study was not high enough for a method designed for routine clinical applications.     

Functional and structural adaptations in the pancreatic α-cell and changes in glucagon signaling during protein malnutrition

Chronic malnutrition leads to multiple changes in β-cell function and peripheral insulin actions to adapt glucose homeostasis to these restricted conditions. However, despite glucose homeostasis also depends on glucagon effects, the role of α-cells in malnutrition is largely unknown. Here, we studied α-cell function and hepatic glucagon signaling in mice fed with low-protein (LP) or normal-protein diet for 8 wk after weaning. Using confocal microscopy, we found that inhibition of Ca2? signaling by glucose was impaired in α-cells of LP mice. Consistent with these findings, the ability of glucose to inhibit glucagon release in isolated islets was also diminished in LP mice. This altered secretion was not related with changes in either glucagon gene expression or glucagon content. A morphometric analysis showed that α-cell mass was significantly increased in malnourished animals, aspect that was probably related with their enhanced plasma glucagon levels. When we analyzed the hepatic function, we observed that the phosphorylation of protein kinase A and cAMP response-binding element protein in response to fasting or exogenous glucagon was impaired in LP mice. Additionally, the up-regulated gene expression in response to fasting observed in the hepatic glucagon receptor as well as several key hepatic enzymes, such as peroxisome proliferator-activated receptor γ, glucose-6-phosphatase, and phosphoenolpyruvate carboxykinase, was altered in malnourished animals. Finally, liver glycogen mobilization in response to fasting and the ability of exogenous glucagon to raise plasma glucose levels were lower in LP mice. Therefore, chronic protein malnutrition leads to several alterations in both the α-cell function and hepatic glucagon signaling.