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The kidney is frequently involved by autoimmune rheumatic diseases. The renal manifestations may be variable, ranging from asymptomatic proteinuria and microscopic haematuria to nephrotic syndrome and rapidly progressive glomerulonephritis or vasculitis. In a number of cases the kidney involvement is related to the treatment of the original disease and may represent a major cause of morbidity and mortality. Thus, it is important for nephrologists and rheumatologists to remember that dysfunction of the kidney may be part of the primary systemic disorder or consequence of its pharmacotherapy. In the first part of this review we will analyse the kidney involvement in four autoimmune connective tissue diseases: systemic lupus erythematosus, Sjögren syndrome, polymyositis/dermatomyositis, and systemic sclerosis. Renal disease is common in lupus and is a main cause of morbidity and mortality. About 10% of patients with Sjögren syndrome may present interstitial nephritis or, more rarely, glomerulonephritis. Myoglobinuria and acute kidney injury is a frequent complication of polymyositis. Renal disease is one of the most serious complications of systemic sclerosis and may present with a dramatic renal crisis, characterized by malignant hypertension, oligo-anuria, and microangiopathic thrombocytopenic anaemia.

Background:Lupus membranous nephropathy (LMN) is a rare disease, usually associated with nephrotic syndrome. Methods:We reviewed the literature by searching for the following terms on Pubmed.gov: lupus nephritis, membranous nephropathy (MN), lupus membranous nephropathy, nephrotic syndrome, and Class V lupus nephritis. Results:The histology of LMN at light microscopy is similar to that of primary MN. Cases of MN associated with focal or diffuse proliferation are not considered LMN by the International Society of Nephrology/Renal Pathology Society classification. Immunofluorescence study of LMN shows deposits of all immunoglobulins and complement. Tubulo-reticular structures, extraglomerular deposits, subepithelial, and scanty subendothelial deposits can be seen on electron microscopy. Phospholipase A2 receptor deposits are usually but not necessarily absent in LMN. The pathogenesis is still not completely understood. The inflammatory milieu of lupus may favor the development of autoantigens and intraglomerular assembly of immune complexes. These are more often associated with mesangial or endocapillary hypercellular lesions. Alternatively, autoantibodies may bind autoantigens in the glomerular subepithelium, triggering a signaling cascade leading to LMN. A central role in the development of podocyte injury and proteinuria is played by the components of complement C5b-C9. CKD progression in LMN is slow but may be accelerated by the frequency of renal flares. Persistent nephrotic syndrome and/or the frequent use of corticosteroids may lead to a series of life-threatening complications. Discussion:Treatment of arterial hypertension, dyslipidemia, and diabetes are of paramount importance. Besides specific therapies of these complications, hydroxychloroquine and vitamin D supplementation are recommended. Immunosuppression should be limited to patients with nephrotic proteinuria. The most frequently used drugs are corticosteroids, calcineurin inhibitors, cyclophosphamide, mycophenolate, and rituximab, alone or combined. Early detection and treatment of renal flares is of paramount importance to prevent CKD progression.

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Accumulating evidence indicates that asymptomatic hyperuricemia is involved in the development of hypertension and chronic kidney disease. A 2-hit model has been proposed to explain the role of urate in hypertension. The first hit entails activation of the renin-angiotensin system and inhibition of nitric oxide synthesis, which promote endothelial dysfunction, proliferation of vascular smooth muscle cells, and sodium reabsorption, leading to a moderate but consistent increase in systemic blood pressure. The second hit involves the immune system. Uric acid released in response to hypertension-induced damage can be recognized as a danger molecule by pattern-recognition receptors, the sentinels of the innate immunity. Downstream signaling from these receptors leads to dendritic cell maturation and activation of resting T cells, but it can also trigger the inflammasome and induce the secretion of proinflammatory cytokines. This proinflammatory milieu concurs in expanding the extracellular fluid volume and in increasing vascular resistances, which further promote systemic hypertension. Through similar mechanisms, hyperuricemia may also cause vascular and tubulointerstitial lesions that favor the development and progression of chronic kidney disease. To counteract these actions, xanthine oxidase inhibitors and uricosuric agents have been advocated as logical candidates to decrease the serum levels of uric acid. However, despite a clear rationale for using hypouricemic drugs in patients with chronic kidney disease, there is currently a lack of robust evidence that lowering uric acid may slow the progression of renal disease.

•The Laser Powder Bed Fusion (L-PBF) ensures high degree in freedom of design.•The volumetric energy density has major influence on the ultimate tensile strength.•Hardness and roughness suffer from a strong anisotropy.•L-PBF is a valid alternative to the traditional die casting process.•The proposed fuzzy model is in a very good agreement with the experimental results.

Leonardo has been involved in the realization of several infrared payloads for Earth observation since 1990. Among the currently in-orbit operative instruments are the two Sea and Land Surface Temperature Radiometers (SLSTRs) and PRISMA (PRecursore IperSpettrale della Missione Applicativa, meaning Hyperspectral Italian Pre-cursor of Operational mission). The SLSTRs are high-accuracy radiometers that provide sea surface temperature data continuity with respect to previous (A)ATSRs in order to serve climatology over the next 20 years, and exist within the framework of the European Space Agency Sentinel-3 mission, which is part of the Copernicus program. The PRISMA program is the first Agenzia Spaziale Italiana optical hyperspectral mission for Earth observation. It is based on a high spectral resolution spectrometer operating in the visible-short wave infrared channels optically integrated with a panchromatic camera.

The coronary sinus Reducer represents a novel therapeutic option with established safety and clinical benefit in the treatment of patients with refractory angina, possibly achieved by enhancing perfusion of myocardial ischemic territories. We report the first case providing insight on how improved perfusion might translate into improved myocardial function as assessed by cardiac magnetic resonance strain imaging, thus suggesting a physiological rationale to test coronary sinus Reducer in the setting of ischemic cardiomyopathy with reduced ejection fraction and adverse remodelling.

ABSTRACTIntroduction: Lipid disorders are frequent after kidney transplantation (KT) and KT recipients are considered at high- or very-high cardiovascular risk. Among many concurring factors, a major role is played by immunosuppressants.Areas covered: General measures to manage lipid disorders first include physical activity and diet counseling. Modulating the doses of immunosuppressants also improves dyslipidemia. When lipid-lowering drugs are necessary to control elevated plasma cholesterol and/or triglycerides, statins are the cornerstone for managing hypercholesterolemia. However, side-effects (e.g. myopathy, new-onset diabetes, and kidney graft dysfunction) may occur. In these cases, ezetimibe (which does not affect kidney function) alone or on top of statins for the severe cases, is suggested by the most recent Guidelines. Proprotein convertase subtilisin/kexin type9 inhibitors are promising but expensive and their use in KT is still limited.Expert opinion: In KT recipients, statins should be used cautiously. Rather than using high-dose statin in difficult patients, an association with ezetimibe is suggested. While fibrates, niacin, and resins do not play a relevant role due to their erratic efficacy and common side-effects, new lipid-lowering drugs are emerging but their safety and efficacy in KT patients still need to be assessed.

The coronary sinus Reducer is a percutaneous device proven to improve angina symptoms in refractory angina (RA). We evaluated its potential cost-effectiveness and impact on the healthcare resource use.

3D anatomical models are becoming a new frontier in surgery for planning and simulation on an individualized patient specific basis. Since 1999, 3D cerebral aneurysms models for neurosurgery have been proposed. The possibility of reproducing in a realistic 3D fashion the malformation with the surrounding vascular structures, provides important preoperative information for the treatment strategy. The same models can be used for training and teaching.

Bitter taste receptors, also known as taste 2 receptors (T2R), are expressed throughout the body and are involved in regulating different physiological processes. T2R expression in the intestinal tract regulates orexigenic and anorexigenic peptide secretion, thus becoming potential a potential target for controlling food intake and the prevalence of obesity and overweight. The present study aims to investigate the implication of hop bitter compounds such as α-acids, β-acids, and xanthohumol in the secretion of anorexigenic hormones and T2R expression in intestinal STC-1 cells. The tested bitter compounds induced the secretion of the anorexigenic hormones glucagon-like peptide 1 and cholecystokinin concurrently with a selective increase of murine Tas2rexpression. Xanthohumol and α-acids selectively increase Tas2r138 and Tas2r130–Tas2r138 expression, respectively, in STC-1 cells, while β-acids increased the expression of all bitter receptors studied, including Tas2r119, Tas2r105, Tas2r138, Tas2r120, and Tas2r130. Increased intracellular calcium levels confirmed this activity. As all investigated bitter molecules increased Tas2r138 expression, computational studies were performed on Tas2r138 and its human orthologue T2R38 for the first time. Molecular docking experiments showed that all molecules might be able to bind both bitter receptors, providing an excellent basis for applying hop bitter molecules as lead compounds to further design gastrointestinal-permeable T2R agonists.