Surgical site infections increase health care costs, morbidity, and mortality in 2% to 5% of surgical patients. Standardised post-surgical surveillance is rare in community settings, causing under-reporting and under-serving of the documented 60% of surgical site infections occurring following hospital discharge. This study evaluated feasibility and concordance (inter-rater reliability) of paired registered nurses using a web-based surveillance tool (how2trakSSI, based on validated guidelines) to detect surgical site infections for up to 30 days after surgery in a cohort of 101 patients referred to Calea Home Care Clinics in Toronto, Canada, March 2015 to July 2016. After paired registered nurse assessors used the tool-less than 10 minutes apart to measure concordance 5 to 7 days postoperatively, they provided feedback on its usefulness at two teleconference discussion groups September 6 to 7, 2016. Overall concordance between assessors was 0.822, remaining consistently above 0.65 across assessor education level and experience, patient age and weight, and wound area. Assessors documented 39.6% surgical site infection prevalence 5 to 7 days after surgery, confirming clinical need, relevance, reliability, and feasibility of using this web-based tool to standardise community surgical site infection surveillance, noting that it was user-friendly, more efficient to use than traditional paper-based tools and useful as a registry for tracking progress.The COVID-19 pandemic caused by SARS-CoV-2 has far-reaching direct and indirect medical consequences. These include both the course and treatment of diseases. It is becoming increasingly clear that infections with SARS-CoV-2 can cause considerable immunological alterations, which particularly also affect pathogenetically and/or therapeutically relevant factors. Against this background we summarize here the current state of knowledge on the interaction of SARS-CoV-2/COVID-19 with mediators of the acute phase of inflammation (TNF, IL-1, IL-6), type 1 and type 17 immune responses (IL-12, IL-23, IL-17, IL-36), type 2 immune reactions (IL-4, IL-13, IL-5, IL-31, IgE), B-cell immunity, checkpoint regulators (PD-1, PD-L1, CTLA4), and orally druggable signaling pathways (JAK, PDE4, calcineurin).  https://www.selleckchem.com/products/cdk2-inhibitor-73.html  In addition, we discuss in this context non-specific immune modulation by glucocorticosteroids, methotrexate, antimalarial drugs, azathioprine, dapsone, mycophenolate mofetil and fumaric acid esters, as well as neutrophil granulocyte-mediated innate immune mechanisms. From these recent findings we derive possible implications for the therapeutic modulation of said immunological mechanisms in connection with SARS-CoV-2/COVID-19. Although, of course, the greatest care should be taken with patients with immunologically mediated diseases or immunomodulating therapies, it appears that many treatments can also be carried out during the COVID-19 pandemic; some even appear to alleviate COVID-19.
  Pegfilgrastim, a pegylated granulocyte colony-stimulating-factor (GCSF), reduces chemotherapy morbidity and mortality in early stage breast cancer. The optimal approach to individual patient selection for GCSF is unknown, in particular whether secondary GCSF should be given after asymptomatic neutropenia, or only after febrile neutropenia (FN).
 
  To determine if preplanned nadir blood counts and subsequent nadir-neutropenia directed GCSF was effective to reduce rates of FN associated with (neo)adjuvant breast cancer chemotherapy. We also aimed to describe (neo)adjuvant chemotherapy and GCSF prescribing practices at our institution.
 
  This was a retrospective electronic medical record review. The rate of FN with secondary GCSF after cycle 1 nadir-neutropenia <1.0 × 10
  cells/L was compared with the rate of FN in patients who did not have cycle 1 nadir blood counts or secondary GCSF, and analyzed according to patient and treatment data.
 
  Between 11/4/2011 and 22/4/2018, 584 patients received (neo)adjuvan in TC and TCH in routine clinical practice should guide primary GCSF use in accordance with international guidelines.
  Cancer emergence is associated with a series of cellular transformations that include acquired drug resistance followed by tumor metastasis. Matrix metalloproteinases (MMPs) and Hsp90 chaperone are implicated in tumor progression, however, they are not studied in the context of drug resistance.
 
  In the present study, we aimed at understanding the cross-talk between acquired drug resistance and tumor progression, linking MMP7 and Hsp90.
 
  We have developed an in vitro model system for acquired drug resistance and studied the correlation between MMP7 and Hsp90. We demonstrate that enhanced drug efflux activity correlates with the induced expression and activity of MMP7, and enhanced metastatic potential of cells, however, in Hsp90-dependent manner. The MMP7 overexpression alone could enhance the drug efflux activity marginally, and metastasis significantly. However, challenging these cells with 17AAG has significantly increased the drug efflux activity and, in contrast, decreased the metastatic potential. Evaluating our in vitro findings in mice xenografts revealed that MMP7 overexpression facilitates altered homing properties. However, these cells, in response to 17AAG treatment, exhibited increased localized tumor growth but decreased tumor metastasis.
 
  We demonstrated a cross-talk between Hsp90 and MMP7 in regulating the acquired drug resistance and tumor progression. Our findings provide novel insights on targeting drug resistant-tumors.
 We demonstrated a cross-talk between Hsp90 and MMP7 in regulating the acquired drug resistance and tumor progression. Our findings provide novel insights on targeting drug resistant-tumors.
  Report the results at 2 years of the patients included in the SENIOR trial.
 
  Patients above 75 years of age represent a fast-growing population in the cathlab. In the SENIOR trial, patients treated by percutaneous coronary intervention (PCI) with drug eluting stent (DES) and a short duration of P2Y12 inhibitor (1 and 6 months for stable and unstable coronary syndromes, respectively) compared with bare metal stents (BMS) was associated with a 29% reduction in the rate of all-cause mortality, myocardial infarction (MI), stroke, and ischaemia-driven target lesion revascularization (ID-TLR) at 1 year. The results at 2 years are reported here.
 
  We randomly assigned 1,200 patients (596[50%] to the DES group and 604[50%] to the BMS group). At 2 years, the composite endpoint of all-cause mortality, MI, stroke and ID-TLR had occurred in 116 (20%) patients in the DES group and 131 (22%) patients in the BMS group (RR 0.90 [95%CI 0.72-1.13], p = .37). IDTLR occurred in 14 (2%) patients in the DES group and 41 (7%) patients in the BMS group (RR 0.