Nosocomial infections, also known as hospital-acquired infections, pose a serious challenge to healthcare professionals globally during the Coronavirus disease 2019 (COVID-19) pandemic. Nosocomial infection of COVID-19 directly impacts the quality of life of patients, as well as results in extra expenditure to hospitals. It has been shown that COVID-19 is more likely to transmit via close, unprotected contact with infected patients. Additionally, current preventative and containment measures tend to overlook asymptomatic individuals and superspreading events. Since the mode of transmission and real origin of COVID-19 in hospitals has not been fully elucidated yet, minimizing nosocomial infection in hospitals remains a difficult but urgent task for healthcare professionals. Healthcare professionals globally should form an alliance against nosocomial COVID-19 infections. The fight against COVID-19 may provide valuable lessons for the future prevention and control of nosocomial infections. The present review will discuss some of the key strategies to prevent and control hospital-based nosocomial COVID-19 infections.

Marfan syndrome (MFS) is a complex connective tissue disease that is primarily characterized by cardiovascular, ocular and skeletal systems disorders. Despite its rarity, MFS severely impacts the quality of life of the patients. It has been shown that molecular genetic factors serve critical roles in the pathogenesis of MFS. FBN1 is associated with MFS and the other genes such as FBN2 , transforming growth factor beta (TGF-β) receptors ( TGFBR1 and TGFBR2 ), latent TGF-β-binding protein 2 ( LTBP2 ) and SKI , amongst others also have their associated syndromes, however high overlap may exist between these syndromes and MFS. Abnormalities in the TGF-β signaling pathway also contribute to the development of aneurysms in patients with MFS, although the detailed molecular mechanism remains unclear. Mutant FBN1 protein may cause unstableness in elastic structures, thereby perturbing the TGF-β signaling pathway, which regulates several processes in cells. Additionally, DNA methylation of FBN1 and histone acetylation in an MFS mouse model demonstrated that epigenetic factors play a regulatory role in MFS. The purpose of the present review is to provide an up-to-date understanding of MFS-related genes and relevant assessment technologies, with the aim of laying a foundation for the early diagnosis, consultation and treatment of MFS.

In this study, a hairpin DNA (hpDNA)-conjugated gold nanocages (GNCs) SERS probe was developed for the long-term detection and imaging of miR-144-3p in osteogenic differentiation of bone marrow stem cells.

Primary congenital glaucoma (PCG) is one of the primary causes of blindness in children and is characterized by congenital trabecular meshwork and anterior chamber angle dysplasia. While being a rare condition, PCG severely impairs the quality of life of affected patients. However, the pathogenesis of PCG remains to be fully elucidated. It has previously been indicated that genetic factors serve a critical role in the pathogenesis of PCG, although patients with PCG exhibit significant genetic heterogeneity. Mutations in the cytochrome P450 family 1 subfamily B member 1 gene have been implicated in PCG and further genes that have been reported to be involved in PCG are myocilin, forkhead box C1, collagen type I α1 chain and latent transforming growth factor β binding protein 2. The present review aims to provide an up to date understanding of the genes associated with PCG and the use of molecular technologies in the identification of such genes and mutations. This may pave the way for the development of preventative methods, early diagnosis and improved therapeutic strategies in PCG.