The current state of knowledge on how to improve skin flap survival: A review.

The incorporation of skin flaps in wound closure management with its cosmetic implications has appeared as a gleam of hope in providing desirable outcomes. Given the influence of extrinsic and intrinsic factors, skin flaps are prone to several complications, including ischemia-reperfusion injury (IRI). Numerous attempts have been undertaken to enhance the survival rate of skin flaps entailing pre/post-conditioning with surgical and pharmacological modalities. Various cellular and molecular mechanisms are employed in these approaches in order to reduce inflammation, promote angiogenesis and blood perfusion, and induce apoptosis and autophagy. With the emerging role of multiple stem cell lineages and their ability to improve skin flap viability, these approaches are increasingly being used to develop even more translationally applicable methods. Therefore, this review aims at providing current evidence around pharmacological interventions for improving skin flap survival and discussing their underlying mechanism of action.

Tumor-promoting myeloid cells in the pathogenesis of human oncoviruses: potential targets for immunotherapy.

Oncoviruses, known as cancer-causing viruses, are typically involved in cancer progression by inhibiting tumor suppressor pathways and uncontrolled cell division. Myeloid cells are the most frequent populations recruited to the tumor microenvironment (TME) and play a critical role in cancer development and metastasis of malignant tumors. Tumor-infiltrating myeloid cells, including tumor-associated macrophages (TAMs), myeloid-derived suppressor cells (MDSCs), tumor-associated dendritic cells (TADCs), and tumor-associated neutrophils (TANs) exert different states from anti-tumorigenic to pro-tumorigenic phenotypes in TME. Although their role in the anti-tumorigenic state is well introduced, their opposing roles, pro-tumorigenic activities, such as anti-inflammatory cytokine and reactive oxygen species (ROS) production, should not be ignored since they result in inflammation, tumor progression, angiogenesis, and evasion. Since the blockade of these cells had promising results against cancer progression, their inhibition might be helpful in various cancer immunotherapies. This review highlights the promoting role of tumor-associated myeloid cells (TAMCs) in the pathophysiology of human virus tumorigenesis.

Reinfection and reactivation of SARS-CoV-2.

As the cases of SARS-CoV-2 infection escalates, the essence of in-depth knowledge around acquired immunity and emergence of reinfection and reactivation have to be captured. While being a rare phenomenon, reinfection occurs as the result of diminishing protection conferred by antibodies, especially IgG. Reactivation is more concerned with the role of various elements including shedding lingering viral RNA for a prolonged time and incomplete resolution of infection along with the insight of dormant viral exosomes' role. The concept of testing positive after two consecutive negative results requires proper discrimination of reinfection from reactivation. In this review, we summarized the current evidence for possible mechanisms leading to viral reactivation or test re-positivity. We also pointed out risk factors associated with both reinfection and reactivation.