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Aims/hypothesis The interplay of ACE and type 2 ACE (ACE2) has been recognised as playing an important role in the tissue renin-angiotensin system within the kidney. In the present study, we measured urinary mRNA expression of ACE and ACE2 in patients with type 2 diabetic nephropathy. Methods We studied 50 patients with diabetic nephropathy: 26 were being treated by ACE inhibitor (ACEI) alone (ACEI group), the other 24 by ACEI and angiotensin-receptor blocker (ARB) (ACEI+ARB group). mRNA expression of ACE and ACE2 was measured by real-time quantitative RT-PCR at 0 and 12 weeks. All patients were then followed for 56 weeks. Results Proteinuria correlated significantly with urinary ACE (r = 0.454, p = 0.001) and ACE2 expression (r = 0.651, p < 0.001). Urinary ACE2 expression correlated with estimated GFR (r = -0.289, p = 0.042). In the ACEI group, there was a significant inverse correlation between the rate of GFR decline and urinary ACE2 expression at baseline (r = -0.423, p = 0.031) as well as at 12 weeks (r = -0.395, p = 0.046). In contrast, there was no significant correlation between the rate of GFR decline and urinary ACE2 expression at baseline or at 12 weeks in the ACEI+ARB group. The rate of GFR decline did not correlate with the baseline urinary ACE expression of either group. Conclusion/interpretation There was a relationship between urinary mRNA expression of ACE2 and the degree of proteinuria. The physiological implication and possibility of clinical application of quantifying urinary ACE2 expression require further study.

Background: Urinary intercellular adhesion molecule-1 (ICAM-1) level is potentially a valuable biomarker of lupus nephritis (LN), but because ICAM-1 is a cell-surface molecule, soluble ICAM-1 level in urinary supernatant measured by ELISA may not be biologically relevant. Methods: The ICAM-1 level in urine sediment of 12 LN patients, 10 patients with pauci-immune necrotizing glomerulonephritis (NecGN), and six healthy controls were determined with a polymerase chain reaction (PCR)-based assay. The urinary sediment levels of miR-221, miR-222, miR-339-3P and miR-339-5P, which are involved in the regulation of ICAM-1 production, were also quantified. Results: LN patients had lower urinary sediment ICAM-1 levels than the other two groups (overall p = 0.034). In addition, urinary sediment ICAM-1 level inversely correlated with the estimated glomerular filtration rate (GFR) (r = −0.474, p = 0.026) but not other markers of lupus activity, or urinary sediment levels of miR-221, miR-222, miR-339-3P, or miR-339-5P. However, serum anti-dsDNA level inversely correlated with urinary sediment levels of miR-221 (r = −0.591, p = 0.043) and miR-222 (r = −0.689, p = 0.013), while urinary sediment miR-221 level also correlated with serum C3 level (r = 0.658, p = 0.02). Conclusions: We conclude that urinary sediment ICAM-1 level was significantly reduced in LN, and the level inversely correlated with renal function. Urinary sediment miR-221 and miR-222 levels correlate with lupus disease activity and may serve as biomarkers of LN.

Polypharmacy, frailty and malnutrition are known predictors of adverse outcomes in dialysis patients. Little has reported about their interaction and composite prognostic values. We aimed to describe the interaction between polypharmacy, frailty, nutrition, hospitalization, and survival in peritoneal dialysis patients. In this prospective cohort study, we recruited 573 peritoneal dialysis patients. Drug burden was measured by medication number and daily pill load. Frailty and nutrition were assessed by the validated Frailty Score (FQ) and Subjective Global Assessment (SGA) respectively. All patients were followed for two years. Primary outcome was all-cause mortality. Secondary outcomes were fall and fracture episodes, hospitalization, change in FQ and SGA. At baseline, each patient took 7.5 ± 2.6 medications with 15.5 ± 8.5 tablets per day. Medication number, but not daily pill load predicted baseline FQ (p = 0.004) and SGA (p = 0.03). Over 2 years, there were 69 fall and 1,606 hospitalization episodes. In addition, 148 (25.8%) patients died, while FQ and SGA changed by 0.73 ± 4.23 and −0.07 ± 1.06 respectively in survivors. Medication number (hospitalization: p = 0.02, survival: p = 0.005), FQ (hospitalization: p < 0.001; survival: p = 0.01) predicted hospitalization and survival. Medication number also predicted fall episodes (p = 0.02) and frailty progression (p = 0.002). Daily pill load did not predict any of these outcomes. Drug burden is high in peritoneal dialysis patients, and it carries important prognostic implication. Medication number but not pill load significantly predicted onset and progression of frailty, malnutrition, fall, hospitalization, and mortality.

Mononuclear cells play a cardinal role in the pathogenesis of systemic lupus erythematosus (SLE). A high urine cytology score has been reported to be associated with lupus nephritis in relapse. The objective of this study was to examine the urinary mononuclear cell population of patients with lupus nephritis, and explore its correlation with lupus disease activity. We studied 12 patients with active lupus nephritis, 17 patients with lupus nephritis in remission, 12 SLE patients with no history of renal disease and 13 healthy subjects. Clinical disease activity was quantified by the SLE Disease Activity Index (SLEDAI). Mononuclear cell species in the urinary sediment were examined by immunocytochemistry. Patients with active lupus nephritis had significantly more mononuclear cells in the urinary sediment. The number of + cell was significantly elevated in the active lupus nephritis than the others (P < 0.001), while there was no significant difference in the number of + and + cell among patient groups. The total urinary mononuclear cell correlated significantly with the overall SLEDAI score (r = 0.58, P < 0.001) as well as the renal score (r = 0.57, P < 0.001). The number of urinary +, but not + or +, cell significantly correlated with the overall SLEDAI score (r = 0.46, P = 0.003) as well as the renal score (r = 0.40, p < 0.011). In nine patients with renal biopsy, the histological activity index correlated with the total urinary mononuclear cell (r = 0.75, P = 0.02), + (r = 0.69, P = 0.04) and + cell (r = 0.69, P = 0.04). We conclude that urinary mononuclear cell was markedly elevated in patients with active lupus, and the urinary mononuclear cell count correlated significantly with the SLEDAI score and histological activity. + and + cells are the major component of urinary mononuclear cell in SLE patients and their number correlates with lupus disease activity.

MicroRNAs circulating in body fluid have been suggested as biomarkers of various diseases. We studied the serum and urinary level of several miRNA species (miR-200 family, miR-205 and miR-192) in patients with systemic lupus erythematosus (SLE). We studied 40 SLE patients. Serum and urinary miRNA levels were determined and compared with that of healthy controls. The serum levels of miR-200a, miR-200b, miR-200c, miR-429, miR-205 and miR-192, and urinary miR-200a, miR-200c, miR-141, miR-429 and miR-192 of SLE patients were lower than those of controls. Glomerular filtration rate (GFR) correlated with serum miR-200b (r = 0.411, p = 0.008), miR-200c (r = 0.343, p = 0.030), miR-429 (r = 0.347, p = 0.028), miR-205 (r = 0.429, p = 0.006) and miR-192 (r = 0.479, p = 0.002); proteinuria inversely correlated with serum miR-200a (r = −0.375, p = 0.017) and miR-200c (r = −0.347, p = 0.029). SLE disease activity index (SLEDAI) inversely correlated with serum miR-200a (r = −0.376, p = 0.017). Serum miR-200b (r = 0.455, p = 0.003) and miR-192 (r = 0.589, p < 0.001) correlated with platelet count, while serum miR-205 correlated with red cell count (r = 0.432, p = 0.005) and hematocrit (r = 0.370, p = 0.019). These pilot results suggested that miRNA may take part in the pathogenesis of SLE. Further studies are needed to validate the role of serum miRNA as a biomarker of SLE.

The Faculty Development Framework of the Academy Steinert7 defines faculty as all individuals involved in teaching and educating learners across the educational continuum (eg, undergraduate, graduate, postgraduate, and continuing professional development), leadership and management within universities, hospitals, and the community, as well as research and scholarship in the health professions (eg, communication sciences, dentistry, nursing, and rehabilitation sciences). In the future, the ILCM will design and implement training workshops guided by the following principles19: * Evidence-informed educational design * Relevant content * Experiential learning with opportunities for practice and application * Opportunities for feedback and reflection * Intentional community building Moreover, a recent systematic review has highlighted key principles for effective faculty development that extend beyond workshops and individual teaching effectiveness. [...]effective faculty development will require sustained support from HKAM and collaboration with stakeholders across all Colleges to ensure that faculty continue to advance their skills after completing workshops. By equipping trainers with the appropriate competencies and skills, the framework ensures that doctors in training receive high-quality education and mentorship, ultimately enhancing patient care and outcomes within the healthcare system.6 Author contributions All authors have contributed equally to the concept, development and critical revision of the manuscript.

[...]CBME requires trainers to master teaching skills that may not be well-known. [...]the alignment of learning and assessment methods with CBME approaches requires educational standards and procedures to be redesigned. [...]PGME is a relatively new discipline with limited academic presence. [...]there is a need to empower Fellows and CME/CPD providers to use methods that support adult learning, and online learning is a particularly promising method for this learning.11Finally, many learners lack the skills and personal attributes needed for self-directed learning; they require support to acquire these abilities.12 Recommendation 5: HKAM and the Colleges should undertake actions to transform CME/CPD, including: (1) devise and deliver a comprehensive communication plan to effectively engage all stakeholders; (2) reform the structure and redesign the standards and procedures of CME requirements and accreditation to align with the new CME paradigm; (3) design and implement FDPs to empower Fellows and possibly other CME providers to use learning methods which support adult learning; (4) nurture the capacities of learners to practise self-directed learning; (5) support the development of online learning through the provision of technology and relevant training in educational practices; and (6) establish partnerships with overseas CME/CPD accreditation bodies.

The IMACE CPGs, defined as “systematically developed statements to assist practitioner and patient decisions about appropriate health care for specific clinical circumstances”,5 are applicable to healthcare professionals and providers across the public and private sectors in Hong Kong. Institute of Medicine, Committee to Advise the Public Health Service on Clinical Practice Guidelines. Gilberto KK Leung 1 † Ronald MK Lam , 2 ‡; Philip WY Chiu 3 ‡; Philip KT Li 1 ‡; William Ho 4 ‡; Tony PS Ko 5 ‡; CS Lau 6 ‡; FC Pang 7 ‡; Governing Board; Institute for Advancement Excellence 1 Hong Kong Academy of Medicine, Hong Kong SAR, China 2 Department of Health, Hong Kong SAR Government, Hong Kong SAR, China 3 Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong SAR, China 4 Hong Kong Private Hospitals Association, Hong Kong SAR, China 5 Hospital Authority, Hong Kong SAR, China 6 Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China 7 Primary Healthcare Commission, Health Bureau, Hong Kong SAR Government, Hong Kong SAR, China