ion of the data can be found in our previous work [1]. Overall, the main intention of this dataset manuscript is to communicate and promote the adoption of the proposed method by researchers and the water industry alike. GSK-3008348 Integrin antagonist This could further advance the method and encourage the assessment of additional ligands or/and pollutants/elements, including heavy metals which are typically found in water. © 2020 The Author(s).Background Osteoporosis and hypertension are frequent and often coexisting diseases among the elderly. Recent studies suggested that both diseases may share the same etiopathology. Moreover, the treatment of hypertension can affect the bone mineral density and worsen osteoporosis. The aim of this cross-sectional study was to assess the prevalence of low bone mass and osteoporosis in postmenopausal Syrian women and investigate their relationship with hypertension and antihypertensive drugs. Methods 813 postmenopausal women were involved in this cross-sectional study, aged between 40 and 96 yrs. Their menopause duration ranged between 1 and 43 yrs. Bone mineral density was measured using a dual-energy X-ray absorptiometry at the total lumbar spine (L1-L4) and left hip. T-score values were used to determine the diagnosis of osteoporosis. The existence of HTN was defined as blood pressure ≥130/85 mmHg or a history of hypertension medication. Results Using the world health organization criteria, 24% had osteoporosis and 45.2% had low bone mass. The incidence of osteoporosis and low bone mass significantly increased with age and menopause duration and decreased with BMI. Prevalence of hypertension was almost equal among the women who had or did not have osteoporosis. However, hypertensive women who used thiazides or beta blockers had higher values of total lumbar BMD compared with the women who did not. Conclusion Hypertension in postmenopausal Syrian women aged over 40 was not found to be associated with osteoporosis. However, the mean total lumbar BMD of the hypertensive women who took thiazide diuretics or beta blocker was found to be increased significantly comparing to the women who did not take either. Copyright © 2020 Nermeen Hijazi and Zaynab Alourfi.Adult-onset Still’s disease (AOSD) is a rare and inflammatory disorder characterized by spiking fever, rash, arthritis, and multisystemic involvement. HLA has been shown to be associated with AOSD; however, it could not explain the innate immunity and autoinflammatory characteristics of AOSD. To assess the genetic susceptibility of AOSD, we conducted a genome-wide association study (GWAS) on a cohort of 70 AOSD cases and 688 controls following a replication study of 36 cases and 200 controls and meta-analysis. The plasma concentrations of associated gene product were determined. The GWAS, replication, and combined sample analysis confirmed that SNP rs11102024 on 5′-upstream of CSF1 encoding macrophage colony-stimulating factor (M-CSF) was associated with AOSD (P = 1.20 × 10-8, OR (95% CI) 3.28 (2.25~4.79)). Plasma levels of M-CSF increased in AOSD patients (n = 82, median 9.31 pg/mL), particularly in the cases with activity score ≥ 6 (n = 42, 10.94 pg/mL), compared to the healthy donors (n = 68, 5.31 pg/mL) (P less then 0.0001). Patients carrying rs11102024TT genotype had higher M-CSF levels (median 20.28 pg/mL) than those with AA genotype (6.82 pg/mL) (P less then 0.0001) or AT genotype (11.61 pg/mL) (P = 0.027). Patients with systemic pattern outcome were associated with elevated M-CSF and frequently observed in TT carriers. Our data suggest that genetic variants near CSF1 are associated with AOSD and the rs11102024 T allele links to higher M-CSF levels and systemic outcome. These results provide a promising initiative for the early intervention and therapeutic target of AOSD. Further investigation is needed to have better understandings and the clinical implementation of genetic variants nearby CSF1 in AOSD. Copyright © 2020 Yi-Ming Chen et al.Atherosclerosis is a multifactorial chronic inflammatory arterial disease forming the pathological basis of many cardiovascular diseases such as coronary heart disease, heart failure, and stroke. Numerous studies have implicated inflammation as a key player in the initiation and progression of atherosclerosis. Galectin-3 (Gal-3) is a 30 kDa β-galactose, highly conserved and widely distributed intracellularly and extracellularly. Gal-3 has been demonstrated in recent years to be a novel inflammatory factor participating in the process of intravascular inflammation, lipid endocytosis, macrophage activation, cellular proliferation, monocyte chemotaxis, and cell adhesion. This review focuses on the role of Gal-3 in atherosclerosis and the mechanism involved and several classical Gal-3 agonists and antagonists in the current studies. Copyright © 2020 Ziyu Gao et al.Objectives To explore effects of Epstein-Barr virus (EBV) infection on CD19+ B lymphocytes in patients with immunorelated pancytopenia (IRP). Methods An enzyme-linked immunosorbent assay (ELISA) in vitro diagnostic kit was used to detect EBV capsid antigen- (CA-) IgG and VCA-IgM antibodies in the serum. We analyzed the EBV-DNA copies of CD19+ B lymphocyte by using real-time quantitative polymerase chain reaction (RT-qPCR). CD21, CD23, CD5, CD80, and CD86 receptors on the surfaces of CD19+ B cells were detected by flow cytometry (FCM). The correlation between these receptors and EBV-DNA copies were evaluated. Results The results revealed that the positive rate of EBVCA-IgM and CD19+ B lymphocyte EBV-DNA copy in the IRP group were significantly higher than those in the control group (P less then 0.05). CD19+ B lymphocyte EBV-DNA copies were also more abundant in IRP patients than in control subjects (P less then 0.05). CD19+ B lymphocyte EBV-DNA copies were also more abundant in IRP patients than in control subjects (P less then 0.05). CD19+ B lymphocyte EBV-DNA copies were also more abundant in IRP patients than in control subjects (. Conclusions EBV infection may activate CD19+ B lymphocytes and further disrupt bone marrow hematopoiesis in IRP patients. Copyright © 2020 Yang Zhao et al.