Five actions for five people: emergency cesarean section protocol.

OBJECTIVE: The scope of this work is to evaluate an operative protocol for emergency C-section to improve teamwork and reduce surgical setup time. METHODS: Sixty-six health care operators working together in the delivery ward (gynecologists, midwives, anesthesiologists) simulated an emergency scenario applying a "five actions for each operator" protocol. For each simulation, the decision to delivery interval was considered and the perception of each operator as a team worker was analyzed with specific tests. RESULTS: The "five actions for five people" protocol significantly reduces the decision to delivery interval (p < 0.001) for emergency C-section. At the same time, a simple and codified scheme improves communication among team members, avoids overlapping roles. Indeed, all the operators become more aware of being helpful to the team (p < 0.001). CONCLUSION: The use of a standardized, simple, and immediately usable protocol improves the performance of the delivery room team in terms of the urgency and quality of the operator's participation in the event. Procedures of this type should be favored within emergency obstetric settings. TRIAL REGISTRATION NUMBER: CEAVNO 19-01-23. Local ethical Committee (COMITATO ETICO REGIONALE PER LA SPERIMENTAZIONE CLINICA - Sezione autonoma Area Vasta Nord Ovest -CEAVNO) approved this study as simulation training study. All the operators participated voluntary during their working time.

Circulating leptin, resistin, adiponectin, visfatin, adipsin and ghrelin levels and insulin resistance in postmenopausal women with and without the metabolic syndrome.

OBJECTIVE: To measure serum levels of adipsin, leptin, resistin, adiponectin, visfatin, ghrelin and insulin in postmenopausal women screened for the metabolic syndrome (METS). METHODS: Serum of 100 postmenopausal women was analyzed using multiplex technology for the mentioned analytes. In addition, values for the homeostasis model assessment of insulin resistance (HOMA-IR) were calculated. Comparisons were performed in accordance to the presence or not of the METS and each of its components. Criteria of the American Heart Association were used to define the METS. RESULTS: Age and time since menopause onset were similar in women with the METS (n=57) as compared to those without the syndrome (n=43). METS women displayed significantly higher levels of adipsin, leptin, resistin, insulin and HOMA-IR values and lower adiponectin levels. These differences were mainly observed among women with abdominal obesity, independent of fulfilling METS criteria or not. In this same sense, lower adiponectin levels significantly related to low HDL-C and high triglyceride levels; and higher insulin and HOMA-IR values related to high triglyceride and glucose levels, respectively. CONCLUSION: In this sample, postmenopausal women with the METS displayed higher insulin and adipokine levels. These were mainly related to abdominal obesity and metabolic and lipid abnormalities. More research is warranted in this regard.

Angiogenesis, inflammation and endothelial function in postmenopausal women screened for the metabolic syndrome.

BACKGROUND: Prevalence of the metabolic syndrome (METS) increases after the menopause; nevertheless, concomitant vascular, inflammatory and endothelial changes have not been completely elucidated. OBJECTIVE: To measure serum markers of angiogenesis, inflammation and endothelial function in postmenopausal women screened for the METS. METHODS: Serum of 100 postmenopausal women was analyzed for angiopoietin-2, interleukin-8 (IL-8), soluble FAS ligand (sFASL), interleukin-6 (IL-6), tumour necrosis factor alpha (TNF-α), soluble CD40 ligand (sCD40L), plasminogen activator inhibitor-1 (PAI-1), and urokinase-type plasminogen activator (uPA). Comparisons were made in accordance to the presence or not of the METS and each of its components. Modified Adult Treatment Panel III criteria were used to define the METS. RESULTS: Women with the METS (n=57) had similar age and time since menopause as compared to those without the syndrome (n=43). In general, women with the METS displayed a trend for higher levels of the analyzed markers. Nevertheless, only IL-6 levels were found to be significantly higher and uPA levels significantly lower among METS women as compared to those without the syndrome. When analyte levels were compared as to presenting or not each of the diagnostic features of the METS, it was found that IL-6 levels were higher among women with abdominal obesity, low HDL-C and high triglyceride levels. Women with low HDL-C and high triglyceride levels presented significantly lower uPA levels and those with high glucose and low HDL-C displayed significantly higher sCD40L levels. CONCLUSION: Postmenopausal women with the METS in this sample displayed higher IL-6 (inflammation) and lower uPA levels (endothelial dysfunction). These were mainly related to metabolic and lipid abnormalities. More research is warranted in this regard.

Expression of NHERF1 in colonic tumors induced by 1,2-dimethylhydrazine in rats is independent of plasma ovarian steroids.

In normal embryonic fibroblasts, the Na(+)/H(+) exchanger regulator factor 1 (NHERF1) stabilizes E-cadherin/ß-catenin binding and the lack of NHERF1 expression promotes cell transformation thus acting as a tumor suppressor gene. We here tested the hypothesis that NHERF1 could act as a tumor suppressor gene in colon cancer as a mediator of estrogens' protective actions in colon carcinogenesis. We studied the expression and localization of NHERF1 and ß-catenin by immunohistochemistry in colonic tumors induced by 1,2 dimethylhidrazine (DMH) in Sprague-Dawley rats. One group of the rats treated with the carcinogen was ovariectomized (OVX) in the middle of the tumor induction, simulating a human menopausal condition. We observed a protective role of estrogens in colon cancer, as non-ovariectomized rats (DMH) had a reduced tumor area compared with the ovariectomized group (DMH + OVX; mean ± SE) 28.98 ± 4.65 vs. 67.58 ± 8.69 (p < 0.00380). Despite the lack of plasma estrogen stimulation, we found abundant expression of NHERF1 in colon tumors from ovariectomized rats. NHERF1 was mainly localized in the cytoplasm of the adenocarcinoma cells and lost the apical localization previously reported in normal colon tissue. We also detected expression of NHERF1 by western blot in the SW48, CACO-2, and HT29 colon cancer cell lines. Non-estrogenic factors in plasma or the tumor microenvironment may regulate NHERF1 expression in transformed colon epithelial cells. Further studies are required to understand the regulation of NHERF1 expression in colon cancer tissue.

P-cadherin and beta-catenin are useful prognostic markers in breast cancer patients; beta-catenin interacts with heat shock protein Hsp27.

The cadherin-catenin proteins have in common with heat shock proteins (HSP) the capacity to bind/interact proteins of other classes. Moreover, there are common molecular pathways that connect the HSP response and the cadherin-catenin protein system. In the present study, we have explored whether in breast cancer the HSP might interact functionally with the cadherin-catenin cell adhesion system. Beta-catenin was immunoprecipitated from breast cancer biopsy samples, and the protein complexes isolated in this way were probed with antibodies against HSP family members. We are thus the first to demonstrate a specific interaction between beta-catenin and Hsp27. However, beta-catenin did not bind Hsp60, Hsp70, Hsp90, gp96, or the endoplasmic reticulum stress response protein CHOP. To confirm the finding of Hsp27-beta-catenin interaction, the 27-kDa immunoprecipitated band was excised from one-dimensional polyacrylamide gel electrophoresis gels and submitted to liquid chromatography-tandem mass spectrometry with electrospray ionization, confirming a role for Hsp27. In addition, beta-catenin interacted with other proteins including heat shock transcription factor 1, P-cadherin, and caveolin-1. In human breast cancer biopsy samples, beta-catenin was coexpressed in the same tumor areas and in the same tumor cells that expressed Hsp27. However, this coexpression was strong when beta-catenin was present in the cytoplasm of the tumor cells and not when beta-catenin was expressed at the cell surface only. Furthermore, murine breast cancer cells transfected with hsp25 showed a redistribution of beta-catenin from the cell membrane to the cytoplasm. When the prognostic significance of cadherin-catenin expression was examined by immunohistochemistry in breast cancer patients (n = 215, follow-up = >10 years), we found that the disease-free survival and overall survival were significantly shorter for patients expressing P-cadherin and for patients showing expression of beta-catenin in the cytoplasm only (not at the cell surface). The interactions of beta-catenin with Hsp27 and with HSF1 may explain some of the molecular pathways that influence tumor cell survival and the clinical significance in the prognosis of the breast cancer patients.