Impact of the Fourth Industrial Revolution on the Health Sector: A Qualitative Study.

OBJECTIVES: The Fourth Industrial Revolution is changing the way health is understood, transforming the methods of treatment and diagnosis as well as the relationship between health professionals and patients and altering the management and organization of health systems. The main objective of this study was to explore the impact that the Fourth Industrial Revolution is having on the health sector. METHODS: Conducting interviews consisting of four questions with 10 professionals who had experience working in the health sector to gain their insights and to obtain information to meet the general objective of the study as well as its specific objectives. RESULTS: From the analysis of the respondents' responses, it was possible to create five dimensions developed by the topics most addressed by respondents, namely, impact on healthcare efficiency and effectiveness, impact on government action, impact on human resources, impact on health system organization, and financial impact on the health sector. CONCLUSIONS: Although the Fourth Industrial Revolution is still at an early stage, it has been concluded that it is having a major positive impact on the health sector. For the effective and efficient implementation of these disruptive technologies, a global interaction between governments, health professionals, stakeholders, and society is essential to make this change possible.

Evaluation of the reactivity of sera from patients with systemic lupus erythematosus against the human MCP1.

This study evaluates metaphase chromosome protein 1 (MCP1), a nuclear antigen, as a diagnostic marker for systemic lupus erythematosus (SLE). Reactivity of sera from 114 Portuguese patients with autoimmune rheumatic disease or from healthy blood donors (HBD), against MCP1, produced in bacteria (bact-MCP1) or in its native form (native-MCP1), was determined by immunoblotting. Predictive and discriminative power of MCP1 reactivity for SLE diagnosis in disease-control groups was evaluated by logistic regression, its diagnostic value determined by receiver-operating characteristic analysis and compared with similar analysis of antinuclear antibody and double-stranded DNA (dsDNA). We demonstrated that native-MCP1, in contrast to bact-MCP1, reacts with SLE sera with significant predictive and discriminative power versus other autoimmune diseases (odds ratio [OR] ≤3.537 and ≥3.265; area under the receiver-operating characteristic curve [AUC] ≤0.643 and ≥0.636) or versus HBD (OR = 5.006; AUC = 0.671), showing a good diagnostic power with high specificity (82.1% versus HBD) and low sensitivity for SLE, similar to those of dsDNA. The reactivity of SLE sera with native-MCP1 was shown to be dependent on the presence of phosphorylated residues. Native-MCP1 was shown to have diagnostic value as a specific marker for SLE diagnosis and, therefore, is a suitable substrate for a new antibody test. The widely reported importance of phosphorylated epitopes as targets for autoantibodies in SLE could also be confirmed for native-MCP1.

Evaluation of peritoneal transport and membrane status in peritoneal dialysis: focus on incident fast transporters.

BACKGROUND/AIM: The determinants of baseline fast solute transport are still unclear. We prospectively investigated the relationship of peritoneal solute transport with markers of inflammation, angiogenesis, and membrane status, with a focus on fast transporters. METHODS: Seventy-one incident peritoneal dialysis patients were assessed with baseline and annual peritoneal equilibration tests, using a 3.86% glucose dialysis solution. Residual renal function and markers of inflammation, including systemic and intraperitoneal interleukin-6 (IL-6), effluent cancer antigen 125 (CA-125), and vascular endothelial growth factor (VEGF) appearance rates (ARs), were investigated. The time course of the dialysate-to-plasma ratio of creatinine (D/P creatinine ratio) and its relationship with the biomarkers were investigated by a mixed linear model. RESULTS: Incident fast/fast average transporters had a similar age, diabetes prevalence, and serum and effluent IL-6 levels, but significantly higher levels of CA-125 and VEGF ARs than the slow/slow average group; the D/P creatinine ratio was not correlated with systemic IL-6, but was correlated with effluent CA-125 AR (r = 0.45, p < 0.0001) and VEGF AR (r = 0.52, p < 0.0001). The D/P creatinine ratio decreased with a U-shaped profile (p = 0.02). Intraperitoneal IL-6 was the significant and positive determinant of the time course of the D/P creatinine ratio (p < 0.0001). Effluent CA-125 decreased with time on peritoneal dialysis (p = 0.013). CONCLUSIONS: Baseline peritoneal fast transport was not associated with systemic inflammation, but was related to peritoneal locally produced substances able to mediate transitory hyperpermeability. The D/P creatinine ratio changed during the follow-up period with a U-shaped profile. This was associated with effluent IL-6 and partly with VEGF. CA-125 decreased throughout the follow-up period.

A new case of autosomal recessive agammaglobulinaemia with impaired pre-B cell differentiation due to a large deletion of the IGH locus.

UNLABELLED: Males with X-linked agammaglobulinaemia (XLA) due to mutations in the Bruton tyrosine kinase gene constitute the major group of congenital hypogammaglobulinaemia with absence of peripheral B cells. In these cases, blockages between the pro-B and pre-B cell stage in the bone marrow are found. The remaining male and female cases clinically similar to XLA represent a genotypically heterogeneous group of diseases. In these patients, various autosomal recessive disorders have been identified such as mutations affecting IGHM, CD79A, IGLL1 genes involved in the composition of the pre-B cell receptor (pre-BCR) or the BLNK gene implicated in pre-BCR signal transduction. In this paper, we report on a young female patient characterised by a severe non-XLA agammaglobulinaemia that represents a new case of Igmu defect. We show that the B cell blockage at the pro-B to pre-B cell transition is due to a large homologous deletion in the IGH locus encompassing the IGHM gene leading to the inability to form a functional pre-BCR. The deletion extends from the beginning of the diversity (D) region to the IGHG2 gene, with all JH segments and IGHM, IGHD, IGHG3 and IGHG1 genes missing. CONCLUSION: alteration in Igmu expression seems to be relatively frequent and could account for most of the reported cases of autosomal recessive agammaglobulinaemia.