Intra-abdominal infections (IAI) are an important cause of morbidity and are frequently associated with poor prognosis, particularly in high-risk patients.The cornerstones in the management of complicated IAIs are timely effective source control with appropriate antimicrobial therapy. Empiric antimicrobial therapy is important in the management of intra-abdominal infections and must be broad enough to cover all likely organisms because inappropriate initial antimicrobial therapy is associated with poor patient outcomes and the development of bacterial resistance.The overuse of antimicrobials is widely accepted as a major driver of some emerging infections (such as C. difficile), the selection of resistant pathogens in individual patients, and for the continued development of antimicrobial resistance globally. The growing emergence of multi-drug resistant organisms and the limited development of new agents available to counteract them have caused an impending crisis with alarming implications, especially with regards to Gram-negative bacteria.An international task force from 79 different countries has joined this project by sharing a document on the rational use of antimicrobials for patients with IAIs. The project has been termed AGORA (Antimicrobials: A Global Alliance for Optimizing their Rational Use in Intra-Abdominal Infections). The authors hope that AGORA, involving many of the world's leading experts, can actively raise awareness in health workers and can improve prescribing behavior in treating IAIs.

Radiation is a mainstay of cancer therapy. Radioresistance is a significant challenge in the treatment of locally advanced, recurrent and metastatic cancers. The mechanisms of radioresistance are complicated and still not completely understood. Exosomes are 40–150 nm vesicles released by cancer cells that contain pathogenic components, such as proteins, mRNAs, DNA fragments, non-coding RNAs, and lipids. Exosomes play a critical role in cancer progression, including cell-cell communication, tumor-stromal interactions, activation of signaling pathways, and immunomodulation. Emerging data indicate that radiation-derived exosomes increase tumor burden, decrease survival, cause radiation-induced bystander effects and promote radioresistance. In addition, radiation can change the contents of exosomes, which allows exosomes to be used as a prognostic and predictive biomarker to monitor radiation response. Therefore, understanding the roles and mechanisms of exosomes in radiation response may shed light on how exosomes play a role in radioresistance and open a new way in radiotherapy and translational medicine. In this review, we discuss recent advances in radiation-induced exosome changes in components, focus on the roles of exosome in radiation-induced bystander effect in cancer and emphasize the importance of exosomes in cancer progression and radioresistance for developing novel therapy.

Infiltration of skin tumours by macrophages is an important step in tumour progression, although the mechanisms of macrophage recruitment to the tumour mass and the subsequent effects on tumour growth are poorly understood. Transfecting a murine regressing skin tumour with the gene for transforming growth factor (TGF)b enabled the tumours to grow progressively in vivo thus allowing us to study the role of this cytokine in tumour growth. Flow cytometry was used to show that TGFb-mediated tumour progression was accompanied by an increase in tumour-associated macrophages (TAM) and a decrease in tumour-infiltrating dendritic cells (DCs). TAM in TGFb-secreting tumours expressed lower levels of major histocompatibility complex II and CD86 compared to DC in control tumours and had a high phagocytic capacity as measured by uptake of latex beads in vivo. Indeed, TGFb was directly responsible not only for the enhanced macrophage phagocytosis but also altering the ratio of antigen-presenting cells to favour macrophages over DC. Our results demonstrate that TGFb recruitment and retention of macrophages at the tumour site enable effective tumour evasion of the host immune system and reinforces the need to target TGFb in human cancer immunotherapy trials.