Regulatory T cells (T reg ) inhibit the generation of host-versus-tumor immunity via suppression of tumor-specific effector T-cell responses and development of immune tolerance to neoplastic cells. The transcription factor forkhead box P3 (FOXP3) is an intracellular key molecule for T reg development and function and is considered to represent the most specific T reg cell marker. Tumor-infiltrating lymphocytes (TILs) are considered to be the primary host immune response against solid tumors. Recent results have shown a correlation between survival and density of TILs in colorectal cancer (CRC) patients. 1 Furthermore, there is accumulating evidence that the type of immune cells, rather than their sheer quantity, controls the efficiency of the host-versus-tumor immune response.2 However, the role of TILs in predicting CRC prognosis remains a matter of ongoing debate. Controversy may arise from the uncertainty concerning the in vivo activity of TILs as well as from the lack of discriminating patients according to the underlying type of genomic instability (microsatellite stable vs. unstable). Approximately 10-15% of sporadic CRC and all cases with hereditary nonpolyposis colorectal cancer (HNPCC) are associated with high frequency of microsatellite instability as a result of inactivation or loss of expression of the mismatch repair (MMR) genes MLH1, MSH2 and MSH6 (so-called MMR-deficient tumors). Compared to the majority of sporadic CRC that are MMR-proficient tumors, MMR-deficient tumors are characterized a priori by a higher frequency of TILs and are associated with significantly improved prognosis. 3 Increasing evidence suggests that regulatory T cells (T reg ) have the ability to inhibit the generation of host-versustumor immunity in the microenvironment of tumors via suppression of tumor-specific effector T-cell responses.4,5 The transcription factor forkhead box P3 (FOXP3) is an intracellular key molecule for T reg development and function and is considered to represent the most specific T reg cell marker so far. [6][7][8] In the majority of solid tumors studied so far, high frequency of tumor-infiltrating FOXP3 þ T reg predicted an impaired patient survival. [7][8][9][10][11][12][13][14][15][16] Paradoxically, increased frequency of T reg was recently found to be associated with improved prognosis in lymphoma patients 17 and also in CRC

Background The influence of in-hospital delay (time between admission and operation) on outcome after appendectomy is controversial. Methods A total of 1,827 adult patients underwent open or laparoscopic appendectomy for suspected appendicitis in eleven Swiss hospitals between 2003 and 2006. Of these, 1,675 patients with confirmed appendicitis were included in the study. Groups were defined according in-hospital delay (B12 vs. [12 h). Results Delay [ 12 h was associated with a significantly higher frequency of perforated appendicitis (29.7 vs. 22.7%; P = 0.010) whereas a delay of 6 or 9 h was not. Size of institution, time of admission, and surgical technique (laparoscopic vs. open) were independent factors influencing in-hospital delay. Admission during regular hours was associated with higher age, higher frequency of co-morbidity, and higher perforation rate compared to admission after hours. The logistic regression identified four independent factors associated with an increased perforation rate: age (B65 years vs. [65 years, odds ratio (OR) 4.5, P \ 0.001); co-morbidity (Charlson index [ 0 vs. Charlson index = 0, OR 2.3, P \ 0.001); time of admission (after hours vs. regular hours, OR 0.8, P = 0.040), in-hospital delay ([12 vs. B12 h, OR 1.5, P = 0.005). Perforation was associated with an increased reintervention rate (13.4 vs. 1.6%; P \ 0.001) and longer length of hospital stay (9.5 vs. 4.4 days; P \ 0.001).Conclusions In-hospital delay negatively influences outcome after appendectomy. In-hospital delay of more than 12 h, age over 65 years, time of admission during regular hours, and the presence of co-morbidity are all independent risk factors for perforation. Perforation was associated with a higher reintervention rate and increased length of hospital stay.

Preoperative comorbidity and smoking were risk factors for respiratory complications, whereas neoadjuvant treatment was not. MIE and the use of thoracic epidural analgesia decreased the risk of respiratory failure. Respiratory failure and ARDS were the only independent factors associated with an increased risk of in-hospital death, whereas anastomotic leakage was not.