Malnutrition is widely prevalent in dialysis (1,2). Malnourished patients show a decrease in lean body mass (LBM) that reflects a depletion of somatic protein stores. LBM measurements are not routinely performed in dialysis patients due to the lack of simple and precise techniques for its determination. Recently, we compared lean mass measurements performed by densitometry and by creatinine kinetics in a group of stable peritoneal dialysis patients (5 females, 1 male; mean age 59 ± 11 years; mean time on peritoneal dialysis 22.5 ± 10.1 months). We also correlated lean mass measurements with laboratory determinations that estimate nutritional status. Densitometry was performed with a Norland XR 26 densitometer (Norland XR26, Madison, WI, U.S.A.) using dynamic filtration (3). To determine LBM by creatinine kinetics, we measured the creatinine production of each patient, estimated from excretion and metabolic degradation (4). Then, on the basis of the relationship that exists between creatinine production and LBM (5), we calculated the LBM that corresponded to the creatinine production of each patient.We found that lean mass determined by densitometry was 37.86 ± 2.17 kg in the females and 46.8 kg in the male. Lean mass by this method represents 49.52% of body weight in the females and 72.04% in the male. Lean mass determined by creatinine kinetics was 38.44 ± 1.46 kg in the females and 44.15 kg in the male, representing 50.50% of body weight in the females and the 68.5% in the male.We found no significant difference and a very good correlation in mean lean mass values between techniques (r = 0.95; p = 0.004) (Figure 1). Lean mass determined by both methods correlated significantly with the height but not with the weight of the patients. No correlations were found between lean mass determinations by both methods and laboratory determinations that estimate nutritional status, such as serum albumin, transferrin, whole lymphocyte count, and serum creatinine. Other studies (6), however, have found that, although the correlation be-

Background Circulating acyl-carnitines (acyl-CNTs) are associated with insulin resistance (IR) and type 2 diabetes (T2D) in both rodents and humans. However, the mechanisms whereby circulating acyl-CNTs are increased in these conditions and their role in whole-body metabolism remains unknown. The purpose of this study was to determine if, in humans, blood cells contribute in production of circulating acyl-CNTs and associate with whole-body fat metabolism. Methods and Results Eight non-diabetic healthy women (age: 47±19 y; BMI: 26±1 kg•m−2) underwent stable isotope tracer infusion and hyperinsulinemic-euglycemic clamp study to determine in vivo whole-body fatty acid flux and insulin sensitivity. Blood samples collected at baseline (0 min) and after 3h of clamp were used to determine the synthesis rate of palmitoyl-carnitine (palmitoyl-CNT) in vitro. The fractional synthesis rate of palmitoyl-CNT was significantly higher during hyperinsulinemia (0.788±0.084 vs. 0.318±0.012 %•hr−1, p=0.001); however, the absolute synthesis rate (ASR) did not differ between the periods (p=0.809) due to ~30% decrease in blood palmitoyl-CNT concentration (p=0.189) during hyperinsulinemia. The ASR of palmitoyl-CNT significantly correlated with the concentration of acyl-CNTs in basal (r=0.992,p<0.001) and insulin (r=0.919,p=0.001) periods; and the basal ASR significantly correlated with plasma palmitate oxidation (r=0.764,p=0.027). Conclusion In women, blood cells contribute to plasma acyl-CNT levels and the acyl-CNT production is linked to plasma palmitate oxidation, a marker of whole-body fat metabolism. Future studies are needed to confirm the role of blood cells in acyl-CNT and lipid metabolism under different physiological (i.e., in response to meal) and pathological (i.e., hyperlipidemia, IR and T2D) conditions.

Major depressive disorder (MDD) is a neuropsychiatric disorder, which remains challenging to diagnose and manage due to its complex endophenotype. In this aspect, circulatory microRNAs (cimiRNAs) offer great potential as biomarkers and may provide new insights for MDD diagnosis. Therefore, we systemically reviewed the literature to explore various cimiRNAs contributing to MDD diagnosis and underlying molecular pathways. A comprehensive literature survey was conducted, employing four databases from 2012 to January 2021. Out of 1004 records, 157 reports were accessed for eligibility criteria, and 32 reports meeting our inclusion criteria were considered for in-silico analysis. This study identified 99 dysregulated cimiRNAs in MDD patients, out of which 20 cimiRNAs found in multiple reports were selected for in-silico analysis. KEGG pathway analysis indicated activation of ALS, MAPK, p53, and P13K-Akt signaling pathways, while gene ontology analysis demonstrated that most protein targets were associated with transcription. In addition, chromosomal location analysis showed clustering of dysregulated cimiRNAs at proximity 3p22-p21, 9q22.32, and 17q11.2, proposing their coregulation with specific transcription factors primarily involved in MDD physiology. Further analysis of transcription factor sites revealed the existence of HIF-1, REST, and TAL1 in most cimiRNAs. These transcription factors are proposed to target genes linked with MDD, hypothesizing that first-wave cimiRNA dysregulation may trigger the second wave of transcription-wide changes, altering the protein expressions of MDD-affected cells. Overall, this systematic review presented a list of dysregulated cimiRNAs in MDD, notably miR-24-3p, let 7a-5p, miR-26a-5p, miR135a, miR-425-3p, miR-132, miR-124 and miR-16-5p as the most prominent cimiRNAs. However, various constraints did not permit us to make firm conclusions on the clinical significance of these cimiRNAs, suggesting the need for more research on single blood compartment to identify the biomarker potential of consistently dysregulated cimiRNAs in MDD, as well as the therapeutic implications of these in-silico insights.

Changing trends in governance have contributed to the development of ‘capacity-building initiatives’ in the third sector to enable them to take a greater role in partnership approaches, service delivery and social entrepreneurship. However, analysts have argued that such initiatives are more likely to serve the interests of professionalised welfare groups rather than engage with communities’ own skills and interests. Drawing on in-depth individual interviews and case studies with those engaged in such activities in minority ethnic organisations in devolved Scotland, this paper reveals that ‘capacity’ is a socially constructed, negotiated process, which benefits some organisations more than others. We identify factors which are likely to either facilitate or hinder the process. While there is consensus among participants that such activities play a useful role in developing organisational capacity, we argue that the responsibility for addressing structural factors including socio-economic disadvantage and racism remains with government.

<p class="Abstract"><em>Phragmites karka</em> has been reported for its anti-inflammatory and analgesic activities. Here, extracts of leaf and rhizome of the plant were individually investigated in CCl₄-induced hepatofibrosis in male Wistar rats by administering CCl₄ intraperitoneally biweekly for 6 weeks.  Afterwards the animals were investigated for liver fibrosis at biochemical, molecular and histological levels, and it showed a profound increase (p&lt;0.001) in elevation of serum levels of transaminases, γ-glutamyl transpeptidase, mRNA expression of α smooth muscle actin, collagen and transforming growth factor beta (TGFβ), and extracellular matrix deposition and perilobular necrosis. Both extracts markedly (p&lt;0.001) decreased the elevated levels of these markers. Histopathological investigations also substantiated the above results by exhibiting a decreased in extracellular matrix deposition in post-treatment animals. In conclusion, both extracts had substantially modified the biochemical and molecular markers of liver fibrosis, in addition to histological improvement in architecture of liver.</p>