The medial sural artery perforator (MSAP) continues to gain popularity. Providing a versatile, thin and pliable alternative for commonly used workhorse flaps, it can be used to reconstruct extremities, with reduced donor site morbidity. This meta-analysis was conducted to analyse the current literature to help identify flap characteristics and outcomes. A systematic review was performed following the preferred reporting items for systematic reviews and meta-analysis (PRISMA) guidelines and a literature search was conducted using Medline, Google Scholar and the Cochrane Library. The aim was to identify the outcomes of free MSAP flap reconstructions of upper and lower limb defects over a 10-year period from January 2010 to July 2020. The data was then tabulated and a meta-analysis was carried out. A total of 11 studies for lower limbs and 7 studies for upper limbs were reviewed and analysed with a total number of 257 patients. Limb reconstructions were primarily due to trauma. The most common site of reconstruction of the upper limb was the hand or wrist and the lower limb was the ankle or feet. The mean length of the flap was 9.6 cm. The mean width was 5.4 cm. The mean pedicle length was 9.7 cm. The mean flap thickness was noted as 5.9 mm. The number of perforators was an average of 1.5. The pedicle’s mean arterial diameter was 1.9 mm (mean) and the vein’s mean arterial diameter was 2.9 mm. 80% of donor sites were closed directly. Overall, the flap success rate was 98%. Our results find the MSAP flap to be a versatile, reliable, functionally and aesthetically good reconstructive option for both lower and upper limb defects with low donor site morbidity.

Immune checkpoint inhibitors (ICIs) have revolutionized cancer therapy by offering durable responses for specific patient populations. The heterogeneity in results among individuals underscores the vital need for reliable predictive biomarkers to guide therapeutic strategies. This review aims to elucidate the current landscape of biomarkers in ICI therapy, focusing on their capability to predict patient responses and guide personalized cancer treatment. We examine both existing and emerging biomarkers—such as programmed death-ligand 1 (PD-L1) expression, tumor mutational burden, circulating tumor DNA, gene expression profiles, and the neutrophil-to-lymphocyte ratio—which provide critical insights into patient classification, therapeutic response monitoring, and identification of resistance mechanisms. Despite their potential, considerable challenges remain, including tumor heterogeneity, variability in biomarker testing, and the complexity and dynamic nature of biomarkers across different tumor types. Progress in multi-biomarker approaches and the use of artificial intelligence demonstrate potential for enhancing prediction precision and facilitating more personalized immunotherapy treatments. Additionally, this review summarizes completed and ongoing clinical trials investigating the effect of predictive biomarkers in directing ICI-based cancer treatments and their ability to tailor therapeutic strategies. In conclusion, the review provides an overview of the role of predictive biomarkers in response to ICI therapy.

Endogenous factors, such as reactive oxygen species, and exogenous factors, including ionizing radiation, ultraviolet light, and chemical agents frequently cause DNA damage. This damage compromises genomic stability, leading to mutations, cellular dysfunction, and diseases such as cancer and neurodegenerative disorders. To counteract these threats, cells utilize DNA repair pathways including direct reversal, base excision repair, nucleotide excision repair, mismatch repair, and double-strand break (DSB) repair. These mechanisms are essential for maintaining genomic integrity and ensuring the accurate transfer of genetic information. Deinococcus radiodurans exhibits extraordinary resistance to DNA-damaging agents through a combination of strategies, including an efficient DNA repair system and specialized DNA damage response proteins. Among these, DdrC is a unique DNA-binding protein that recognizes and stabilizes damaged DNA, preventing single-strand breaks from escalating into DSBs. Structural studies show that DdrC functions as a dimer with two distinct DNA-binding sites, enabling it to scan DNA for lesions and compact damaged regions. This compaction not only stabilizes DNA but also aids in preserving nucleoid integrity under extreme ­conditions. The ability of DdrC to bind and compact damaged DNA suggests potential applications in medicine and biotechnology. In cancer therapy, DdrC could disrupt repair mechanisms in tumor cells, enhancing the effects of existing treatments. Its role in stabilizing DNA makes it a candidate for mitigating age-related genomic instability and protecting neurons in neurodegenerative diseases. However, challenges remain, including its bacterial origin, the need for adaptation to human systems, and the development of precise delivery methods. This review provides an overview of DNA damage and repair mechanisms, the properties of DdrC, and its potential for advancing DNA repair-based therapies. While further research is required, DdrC represents a promising step toward innovative approaches to addressing genomic instability.