Lymph node retrieval in pancreaticoduodenectomy specimens: does educating the pathologist matter?

Background:Many previous studies have suggested that the number of lymph nodes retrieved should serve as a benchmark for assessing the adequacy of the resection. The aim was to retrospectively observe the impact of nodal retrieval after educating the pathologist.Methods:Patients undergoing a pancreaticoduodenectomy (PD) between September 2005 and March 2009 were included in the study. The PDs performed between September 2005 and March 2008 were designated as Group A. The pathologistswere educated regarding the importance of nodal counts in PD by the surgeon on the 1st April 2008. PDs performed betweenApril 2008 and March 2009 were designated as Group B.Results:Ninety-eight PDs performed by a single surgeon (D.R.J.) for peri-ampullary malignancy were evaluated. The median number of lymph nodes retrieved in Group A was 11(3–32) nodes. The median number of lymph nodes retrieved in Group B was 22 (10–29) nodes (P < 0.001).The lymph node ratio (positive/total nodes), median number of positive nodes retrieved, and the node positivity (node positive compared to node negative) rate did not change.Discussion:A single intervention with the pathologists did impact the number of lymph nodes retrieved from PD specimens. However, the lymph node ratio and lymph node positivity rate remained unchanged. The pathologist is critical to nodal retrieval in PD, but the use of this lymph node number for benchmark of surgical adequacy may be simplistic.     

Unusual suspects: Real-time physiological evaluation of stressors during laparoscopic donor nephrectomy

IntroductionThe purpose of this study was to document the variability of faculty surgeon electrodermal activity (EDA) peaks during laparoscopic donor nephrectomy (LDN) to determine the effect of case difficulty and learner expertise on the stress response.MethodsEDA for a single faculty surgeon was captured over 15 LDN cases using an Empatica E4 wristband. During each case, one of three transplant fellows (novice, intermediate, or expert level LDN expertise) participated. Difficulty was rated preoperatively as “low/moderate/high” by the faculty. EDA peaks were collected and analyzed; the frequency and magnitude of EDA peaks, case difficulty, and fellow expertise were compared using a two-way factorial ANOVA.ResultsThe main effects of learner expertise (F[2, 308]=11.27, p<0.001) and difficulty rating (F[2, 414]=15.13, p<0.001) were significant. The interaction between difficulty and expertise on faculty EDA peaks was also significant (F[3, 391]=14.29, p<0.001). The novice fellow resulted in higher faculty EDA levels compared to intermediate and expert fellows on low-difficulty cases, but not moderate- or high-difficulty cases.ConclusionsThis is the first report examining faculty surgeon EDA across cases of varying difficulty and varying learner expertise during a high-stakes operation. EDA levels were inversely proportional to the expertise of the learner and case difficulty, suggestive of a significant impact of learner autonomy on faculty stress response.     

Chagasic Megacolon and Proximal Jejunum Microbiota

Background: Among other factors, control of jejunal microflora depends on intestinal emptiness, and it can be impaired by Chagas disease. This study was developed to identify the microecology of the proximal jejunum in chagasic megacolon. Our objective was to characterize both the jejunal microbial stasis before surgery and the microflora after surgical treatment in patients with chagasic megacolon. Methods: The intestinal fluids were collected, and the proximal jejunum microflora was analyzed. Results: Preoperative microflora had shown an increase in bacteria compatible with bacterial overgrowth syndrome, mainly facultative and strict anaerobes microorganisms and fungi. The microflora had changed in the postoperative period in 83% of these patients, with significant decrease in the number of transient microorganisms. Conclusions: Chagasic megacolon was related to an increase in jejunal microflora. By removing the impairment of the colon there was a transient decrease in the proximal jejunum microflora.     

Insulin-Like Growth Factor Pathway–Targeted Therapy in Breast Cancer

The insulin-like growth factor (IGF) pathway plays an important role in cancer development, survival, metastasis, and resistance to antineoplastic therapies in various malignancies. Components of the IGF pathway are potential targets for novel anticancer therapy. In breast cancer, preclinical and clinical data suggest that IGF signaling is critical for tumor growth and resistance to therapy, leading to poor prognosis. There is also evidence of cross-talk between IGF, estrogen, erbB, and mTOR pathways; a potential mechanism of cancer resistance to hormonal or HER2-targeted therapy. This review discusses the rationale and strategies being evaluated in the clinical development of targeting the IGF pathway. It highlights the potential interactions between the IGF pathway and other therapies in breast cancer, and also focuses on the completed and ongoing clinical trials of different IGF pathway–targeted therapies in breast cancer.     

Suppressor of cytokine signaling-3 Provides a novel interface in the cross-talk between angiotensin II and insulin signaling systems

Angiotensin II inhibits insulin-induced activation of phosphatidylinositol 3-kinase through a mechanism, at least in part, dependent on serine phosphorylation of the insulin receptor and insulin receptor substrates (IRS)-1/2. Recent evidence shows that suppressor of cytokine signaling-3 (SOCS-3) is induced by insulin and angiotensin II and participates in the negative control of further stimulation of each of these signaling systems independently. In the present study, we evaluated the interaction of angiotensin II-induced SOCS-3 with the insulin signaling pathway in the heart of living rats. A single iv dose of angiotensin II promotes a significant increase of SOCS-3 in heart, an effect that lasts up to 180 min. Once induced, SOCS-3 interacts with the insulin receptor, JAK-2, IRS-1, and IRS-2. The inhibition of SOCS-3 expression by a phosphorthioate-modified antisense oligonucleotide partially restores angiotensin II-induced inhibition of insulin-induced insulin receptor, IRS-1 and IRS-2 tyrosine phosphorylation, and IRS-1 and IRS-2 association with p85-phosphatidylinositol 3-kinase and [Ser473] phosphorylation of Akt. Moreover, the inhibition of SOCS-3 expression partially reverses angiotensin II-induced inhibition of insulin-stimulated glucose transporter-4 translocation to the cell membrane. These results are reproduced in isolated cardiomyocytes. Thus, SOCS-3 participates, as a late event, in the negative cross-talk between angiotensin II and insulin, producing an inhibitory effect on insulin-induced glucose transporter-4 translocation.