Some ceramics, such as Bioglass, sintered hydroxyapatite, and glass-ceramic A-W, spontaneously form a bone-like apatite layer on their surface in the living body, and bond to bone through the apatite layer. These materials are called bioactive ceramics, and are clinically important for use as bone-repairing materials. However, they cannot be used at high-load sites, such as is found in femoral and tibial bones, because their fracture toughness values are not as high as that of human cortical bone. Titanium metal and its alloys have high fracture toughness, and form a sodium titanate layer on its surface when soaked in a 5 M-NaOH solution at 60 degrees C for 24 h, followed by a heat treatment at 600 degrees C for 1 h. On moving toward the metal interior, the sodium titanate layer gradually changes into the pure metal within a distance of 1 microm from the surface. The mechanical strength of the titanium metal or a titanium alloy is not adversely affected by these chemical and thermal treatments. The titanium metal and its alloys resulting from the above treatment can release Na+ ions from its surface into a surrounding body fluid via an ion exchange reaction with H3O+ ions, resulting in many Ti-OH groups forming on its surface. These Ti-OH groups initially combine with Ca2+ ions to form amorphous calcium titanate in the body environment, and later the calcium titanate combines with phosphate ions to form amorphous calcium phosphate. The amorphous calcium phosphate eventually transforms into bone-like apatite, and by this process the titanium metals are soon tightly bonded to the surrounding living bone through the bone-like apatite layer. The treated metals have already been subjected to clinical trials for applications in artificial total hip joints. Metallic tantalum has also been found to bond to living bone after it has been subjected to the NaOH and heat treatment to form a sodium tantalate layer on its surface.

Limitations of the current therapeutic approach have raised the need for a novel therapeutic agent in breast cancer. Recently, interest in drugs targeting the tumor microenvironment (TME) had drawn attention in the treatment of breast cancer. Furthermore, recent studies have suggested the role of adipocytes, which are part of the TME, in tumor initiation, growth, and metastasis. In this study, we investigated the metabolic interaction between adipocytes and breast cancer cells and its potential as a new therapeutic target in breast cancer. Breast cancer cell lines and human breast cancer tissue samples were evaluated. Compared to cancer cells cultured alone, or the control group, those co-cultured with adipocytes showed lipid transfer from adipocytes to cancer cells and it was different according to the molecular subtype of breast cancer. Breast cancer cells affected the lipolysis of adipocytes and adipocytes affected the β-oxidation of breast cancer cells. The key molecule of the process was fatty acid binding protein 4 (FABP4), which is combined with free fatty acid (FFA) and supports its migration to cancer cells. When FABP4 was suppressed, lipid transfer between adipocytes and cancer cells, lipolysis of adipocytes, and β-oxidation of breast cancer cells were reduced. Furthermore, the expression of lipid metabolism-related proteins and lipolysis-related proteins in breast cancer with adipose stroma showed significantly different expression according to the region of breast cancer tissue. Taken together, we demonstrated the metabolic interaction between adipocytes and breast cancer cells. Breast cancer cells increase the lipolysis in adipocytes and produce a fatty acid, and fatty acid enters into cancer cells. Also, adipocytes contribute to the survival and growth of cancer cells through increased mitochondrial β-oxidation by using fatty acid from adipocytes. The key molecule of the process is FABP4 and when FABP4 is suppressed, the metabolic interaction is reduced, suggesting its role as a potential therapeutic target.

Background Inflammatory bowel disease (IBD) has a risk of venous thromboembolism (VTE) compared with healthy controls, which justify prophylaxis in practice. There are few data on VTE in Asian IBD patients including Koreans. We aimed to investigate the incidence of VTE and the potential risk factors in Korean IBD patients. Methods A nationwide population-based cohort study was performed using claims data from the National Health Insurance service in Korea for 10 years, from 2006 to 2015. VTE, Crohn’s disease (CD) and ulcerative colitis (UC) were operationally defined by using ICD-10 codes, codes for Rare and Intractable Diseases registration, and pharmaceutical prescriptions for IBD-specific drugs. Control group was defined as age- and sex-matched health insurance subscribers without IBD for the same period. The hazard ratio (HR) for the risk of VTE was calculated after adjusting for covariates such as age, sex, rural area, comorbidities, Charlson Comorbidity Index (CCI), admission, and therapeutic drugs use for IBD using multivariate Cox proportional hazard regression. Results A total of 45,037 patients were diagnosed with IBD (13,850 CD and 31,187 UC), and 133,019 were defined as controls. VTE occurred in 411 (0.91%) in IBD, 106 (0.76%) in CD, and 305 (0.98%) in UC, whereas 641 (0.48%) in controls. In univariate analysis among IBD patients, old age (>59 years: HR = 6.256), female sex (HR = 1.537), low income (HR = 1.3090), high CCI (>3 score: HR = 4.053), steroid use (HR = 1.872), emergency care (HR = 1.513) and hospitalisation (HR = 1.352) significantly increased a risk of VTE. However, anti-TNF agent use (HR = 0.611) significantly decreased a risk of VTE. In multivariate analysis with adjustment among all subjects, CD (HR = 15.833) and UC (HR = 8.125) significantly increased a risk of VTE compared with controls. Conclusion Our study demonstrates that VTE is significantly high in Korean IBD patients compared with controls. In addition, old age, female sex, low income, high CCI, steroid use, emergency care, and hospitalisation are suggested as risk factors of VTE in IBD. Interestingly, use of anti-TNF agents may reduce risk of VTE, which should be considered for prophylaxis strategy suitable for Korean IBD patients.

Background Several studies suggested association between inflammatory bowel disease (IBD) and risk of cervical cancer in women. We investigated the risk of cervical cancer in patients with ulcerative colitis (UC) using the nationwide population-based claims data in South Korea. Methods We analysed the claims data of the Korean National Health Insurance (2006–2015). UC and cervical cancer were defined using International Classification of Diseases-10 codes and UC-specific prescription. Age- and sex-matched individuals without UC (control group) were randomly selected from the general population. Hazard ratios (HRs), adjusted for different covariates, were calculated using multivariate Cox proportional hazard regression. Results In total, 30,546 and 88,829 individuals with UC and without UC, respectively, were enrolled. Cervical cancer developed in 26 (0.21%) among UC patients, and 51 (0.14%) among control group, respectively. The standardized incidence ratio (SIR) of cervical cancer in the UC and non-UC groups were 2.04(95% confidence interval [CI], 1.33–2.98), and 1.35(95% CI, 1.00–1.77). The HR of cervical cancer in UC group, with reference to the non-UC group, was 1.56 (95% CI, 0.97–2.50). Further, UC groups were stratified according to age (HR=9.89, 1.62, 0.79 and 3.65 for 0–19, 20–39, 40–59, and ≥60 years, respectively). HR was significantly higher for early-onset UC (0–19 years) and late-onset UC (≥60 years). Among UC, age≥40, low socioeconomic status, rural residence, cerebral vascular disease are risk factors for cervical cancer. Conclusion UC patients had an increased risk of cervical cancer, especially with early-onset (0–19 years) and late-onset (>59 years). Since cervical cancer incidence is higher in UC patients than in the general population, UC patients should receive the human papillomavirus vaccine prophylactically.