Search

The aquaculture sector plays a vital role in global food security, yet it grapples with significant challenges posed by infectious diseases. Piscine lactococcosis is one of the significant threats in rainbow trout aquaculture due to its potential to cause severe economic losses through mortalities, reduced growth rates, and increased susceptibility to other pathogens. It poses challenges in disease management strategies, impacting the sustainability and profitability of rainbow trout farming. The current study focuses on the variations in serum blood parameters of farmed rainbow trout Oncorhynchus mykiss during a lactococcosis outbreak caused by Lactococcus garvieae. Blood samples were collected for biochemical analysis, fish were examined for parasites and bacteria, and DNA from bacterial colonies was PCR‐amplified and sequenced for identification. Overall, 13 biochemical parameters, including proteins, enzymes, lipids, chemicals, and minerals, were measured in serum blood samples from both diseased and healthy fish. The results indicate significant alterations in the levels of these parameters during the outbreak, highlighting the impact of infections on the blood profile of farmed rainbow trout. Urea levels were significantly higher in diseased fish compared to controls, and creatinine, phosphorus, and magnesium also showed similar trends. Alanine aminotransferase and total protein levels were higher in control fish. Chloride levels differed significantly between groups. Iron levels were higher in controls and lower in diseased fish. No significant differences were found in other parameters. This study reveals significant changes in serum blood parameters of rainbow trout during a lactococcosis outbreak caused by L. garvieae. These changes highlight the potential of these parameters as tools for monitoring health status, stress, and aquaculture management. Continuous monitoring can provide valuable insights into disease severity and overall fish health, aiding in the development of improved management practices. The presented data contribute to understanding the pathophysiology of piscine lactococcosis and developing effective mitigation strategies for farmed rainbow trout. [ABSTRACT FROM AUTHOR]

Aims: Systemic inflammatory response, identified by increased total leucocyte counts, was shown to be a strong predictor of mortality after transcatheter aortic valve implantation (TAVI). Yet the mechanisms of inflammation‐associated poor outcome after TAVI are unclear. Therefore, the present study aimed at investigating individual inflammatory signatures and functional heterogeneity of circulating myeloid and T‐lymphocyte subsets and their impact on 1 year survival in a single‐centre cohort of patients with severe aortic stenosis undergoing TAVI. Methods and results: One hundred twenty‐nine consecutive patients with severe symptomatic aortic stenosis admitted for transfemoral TAVI were included. Blood samples were obtained at baseline, immediately after, and 24 h and 3 days after TAVI, and these were analysed for inflammatory and cardiac biomarkers. Myeloid and T‐lymphocyte subsets were measured using flow cytometry. The inflammatory parameters were first analysed as continuous variables; and in case of association with outcome and area under receiver operating characteristic (ROC) curve (AUC) ≥ 0.6, the values were dichotomized using optimal cut‐off points. Several baseline inflammatory parameters, including high‐sensitivity C‐reactive protein (hsCRP; HR = 1.37, 95% CI: 1.15–1.63; P < 0.0001) and IL‐6 (HR = 1.02, 95% CI: 1.01–1.03; P = 0.003), lower counts of Th2 (HR = 0.95, 95% CI: 0.91–0.99; P = 0.009), and increased percentages of Th17 cells (HR = 1.19, 95% CI: 1.02–1.38; P = 0.024) were associated with 12 month all‐cause mortality. Among postprocedural parameters, only increased post‐TAVI counts of non‐classical monocytes immediately after TAVI were predictive of outcome (HR = 1.03, 95% CI: 1.01–1.05; P = 0.003). The occurrence of SIRS criteria within 48 h post‐TAVI showed no significant association with 12 month mortality (HR = 0.57, 95% CI: 0.13–2.43, P = 0.45). In multivariate analysis of discrete or dichotomized clinical and inflammatory variables, the presence of diabetes mellitus (HR = 3.50; 95% CI: 1.42–8.62; P = 0.006), low left ventricular (LV) ejection fraction (HR = 3.16; 95% CI: 1.35–7.39; P = 0.008), increased baseline hsCRP (HR = 5.22; 95% CI: 2.09–13.01; P < 0.0001), and low baseline Th2 cell counts (HR = 8.83; 95% CI: 3.02–25.80) were significant predictors of death. The prognostic value of the linear prediction score calculated of these parameters was superior to the Society of Thoracic Surgeons score (AUC: 0.88; 95% CI: 0.78–0.99 vs. 0.75; 95% CI: 0.64–0.86, respectively; P = 0.036). Finally, when analysing LV remodelling outcomes, ROC curve analysis revealed that low numbers of Tregs (P = 0.017; AUC: 0.69) and increased Th17/Treg ratio (P = 0.012; AUC: 0.70) were predictive of adverse remodelling after TAVI. Conclusions: Our findings demonstrate an association of specific pre‐existing inflammatory phenotypes with increased mortality and adverse LV remodelling after TAVI. Distinct monocyte and T‐cell signatures might provide additive biomarkers to improve pre‐procedural risk stratification in patients referred to TAVI for severe aortic stenosis. [ABSTRACT FROM AUTHOR]

Percutaneous pulmonary valve implantation (PPVI) is nowadays an accepted treatment option to repair post-surgical conduit dysfunction of the right ventricular outflow tract (RVOT). In addition, many patients need a pulmonary valve to reconstruct a hemodynamically incompetent native or conduit free outflow tract. Based on our experience with percutaneous stent-valve placement in a cohort of 125 patients, we report here transvenous reconstruction of a conduit-free, patch repaired outflow tract by utilizing balloon-expandable stent-valves in 23 patients with a median age of 22 years (5-60 years). In 20 patients, the step-by-step procedure was performed uneventful with the aimed success. Severe RVOT dysfunction in term of a clinical relevant regurgitation could be changed to mild, as it was confirmed by follow-up color Doppler echocardiography. In a 5-year-old girl a Melody® valve was placed as a surgical-interventional hybrid approach. In one patient, the procedure was complicated by stent embolization during preparation of the RVOT for stent-valve implantation. Reposition of the embolized stent was nevertheless successful for finishing percutaneous valve-implantation. In one patient, surgical approach became necessary because of the inability to advance the balloon-mounted stent-valve through a pre-stented RVOT. Considering the current available balloon-expandable stent-valves, transvenous pulmonary valve implantation is feasible to treat even an incompetent conduit-free RVOT. However, preparation of the RVOT by pre-stenting, in most patients with more than two stents in telescope technique remains challenging. Reconstruction of RVOT by the current available valves is promising only for a carefully selected group of patients. [ABSTRACT FROM AUTHOR]

The following study demonstrated that, in in vitro differentiated neurons, SIRT1 silencing induced an increase of IGF-1 protein expression and secretion and of IGF-1R protein levels which, in turn, prolonged neuronal cell survival in presence of an apoptotic insult. On the contrary, SIRT1 overexpression increased cell death. In particular, IGF-1 and IGF-1R expression levels were negatively regulated by SIRT1. In SIRT1 silenced cells, the increase in IGF-1 and IGF-1R expression was associated to an increase in AKT and ERK1/2 phosphorylation. Moreover, neuronal differentiation was reduced in SIRT1 overexpressing cells and increased in SIRT1 silenced cells. We conclude that SIRT1 silenced neurons appear more committed to differentiation and more resistant to cell death through the activation of IGF-1 survival pathway. J. Cell. Physiol. 228: 1754-1761, 2013. © 2013 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Aims Several studies have shown that muscle mass loss is an important pathogenic issue in heart failure (HF). Atrogin-1 is a F-box protein selectively expressed in cardiac and skeletal muscle tissue, which plays a pivotal role in muscle wasting regulation. The aim of this study was to investigate the expression of Atrogin-1 and the molecular pathway involved in Atrogin-1 regulation in human HF. Methods and results Cardiac tissue from patients with HF (HF group: n = 10) or with normal left ventricular function (control group: n = 9) was studied by western blot and real time-PCR analysis. Linear regression analysis between patients left ventricular ejection fraction (LVEF) and Atrogin1 or its regulator Forkhead box O 3a (Foxo3a) myocardial expression was performed to test correlations between protein expression and LVEF. Western blot analysis revealed that the myocardial expression of Atrogin-1 in the HF group was 2.5-fold increased compared with controls (P = 0.007). Accordingly, Atrogin-1 mRNA was 1.5 higher than in controls (P = 0.003). The expression of Foxo3a and its up-stream regulator AKT were also measured. Western blot analysis demonstrated in the HF group a 2.56-fold reduction of AKT phosphorylation and a 3.32-fold increase of Foxo3a as compared with controls (P = 0.002 and P = 0.001, respectively). Finally, linear regression showed a significant relationship between Foxo3a or Atrogin-1 expression and LVEF (R = 0.976, P < 0.0001 and R = 0.895, P = 0.003, respectively). Conclusion Our results suggest that in human HF, the activity of AKT decreases, with activation of Foxo3a and induction of Atrogin-1, thereby leading to a molecular state that favours heart muscle loss and left ventricular dysfunction. [ABSTRACT FROM AUTHOR]

The minor salivary glands in the hard palate and the submandibular gland of the Rhesus monkey were subjected to a liquid nitrogen, direct-spray, one-cycle freeze. A 4-min freeze in the temperature range of -40°C to -60°C was used. The extent of tissue destruction was determined at intervals up to 1 year. Clinically relevant findings resulted and form the basis for subsequent studies by this group of investigators. [ABSTRACT FROM AUTHOR]