Objectives: Smart hospitals involve the application of recent information and communications technology (ICT) innovations to medical services; however, the concept of a smart hospital has not been rigorously defined. In this study, we aimed to derive the definition and service types of smart hospitals and investigate cases of each type. Methods: A literature review was conducted regarding the background and technical characteristics of smart hospitals. On this basis, we conducted a focus group interview with experts in hospital information systems, and ultimately derived eight smart hospital service types.Results: Smart hospital services can be classified into the following types: services based on location recognition and tracking technology that measures and monitors the location information of an object based on short-range communication technology; high-speed communication network-based services based on new wireless communication technology; Internet of Things-based services that connect objects embedded with sensors and communication functions to the internet; mobile health services such as mobile phones, tablets, and wearables; artificial intelligence-based services for the diagnosis and prediction of diseases; robot services provided on behalf of humans in various medical fields; extended reality services that apply hyper-realistic immersive technology to medical practice; and telehealth using ICT. Conclusions: Smart hospitals can influence health and medical policies and create new medical value by defining and quantitatively measuring detailed indicators based on data collected from existing hospitals. Simultaneously, appropriate government incentives, consolidated interdisciplinary research, and active participation by industry are required to foster and facilitate smart hospitals.

Radiomics has been spotlighted as imaging biomarker for estimation of intratumoral heterogeneity (ITH) which is regarded as the main reason for resistance to tumor treatment. Although a number of studies has shown clinical evidences that separate measurement of metabolic ITH by texture features (TFs) on ¹⁸F-fluorodeoxyglucose positron emission tomography/computed tomography (¹⁸F-FDG PET/CT) has prognostic ability in various tumors, there has been no consensus regarding the best parameter representing ITH. Besides, it is yet uncertain that TFs are useful for estimation of histopathologic markers, prediction of response to neoadjuvant chemotherapy (NAC), or prognostic ability in breast cancer. To depart from the traditional approach, we evaluated the clinical usefulness of integrated metabolic radiomics using unsupervised clustering with 109 TFs measured from pretreatment ¹⁸F-FDG PET/CT scans of 73 patients with locally advanced breast cancer (LABC) underwent NAC before surgery. Our study shows that metabolic radiomics patterns of LABC are associated with Ki67 expression, achievement of pathologic complete response after NAC, and risk of recurrence. Integrated metabolic radiomics has potential for clinically relevant pretreatment biomarker with predictive and prognostic ability for personalized management in LABC.

Hutchinson-Gilford progeria syndrome (HGPS) is a rare autosomal dominant genetic disease that is caused by a silent mutation of the LMNA gene encoding lamins A and C (lamin A/C). The G608G mutation generates a more accessible splicing donor site than does WT and produces an alternatively spliced product of LMNA called progerin, which is also expressed in normal aged cells. In this study, we determined that progerin binds directly to lamin A/C and induces profound nuclear aberrations. Given this observation, we performed a random screening of a chemical library and identified 3 compounds (JH1, JH4, and JH13) that efficiently block progerin–lamin A/C binding. These 3 chemicals, particularly JH4, alleviated nuclear deformation and reversed senescence markers characteristic of HGPS cells, including growth arrest and senescence-associated β-gal (SA–β-gal) activity. We then used microarray-based analysis to demonstrate that JH4 is able to rescue defects of cell-cycle progression in both HGPS and aged cells. Furthermore, administration of JH4 to Lmna^G609G/G609G-mutant mice, which phenocopy human HGPS, resulted in a marked improvement of several progeria phenotypes and an extended lifespan. Together, these findings indicate that specific inhibitors with the ability to block pathological progerin–lamin A/C binding may represent a promising strategy for improving lifespan and health in both HGPS and normal aging.

Elucidating the molecular mechanisms by which tumors become resistant to Herceptin is critical for the treatment of Her2-overexpressed metastatic breast cancer.