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In this narrative review, we focus on the application of artificial intelligence in the clinical history of patients with glomerular disease, digital pathology in kidney biopsy, renal ultrasonography imaging, and prediction of chronic kidney disease (CKD). With the development of natural language processing, the clinical history of a patient can be used to identify a computable phenotype. In kidney pathology, digital imaging has adopted innovative deep learning algorithms (DLAs) that can improve the predictive capability of the examined lesions. However, at this time, these applications can only be used in research because there is no recognized validation to replace the conventional diagnostic applications. Kidney ultrasonography, used in the clinical examination of patients, provides information about the progression of kidney damage. Machine learning algorithms (MLAs) with promising results for the early detection of CKD have been proposed, but, still, they are not solid enough to be incorporated into the clinical practice. A few tools for glomerulonephritis, based on MLAs, are available in clinical practice. They can be downloaded on computers and cellular phones but can only be applied to uniracial cohorts of patients. To improve their performance, it is necessary to organize large consortia with multiracial cohorts. Finally, in many studies MLA development has been carried out using retrospective cohorts. The performance of the models might differ in retrospective cohorts compared to real-world data. Therefore, the models should be validated in prospective external large cohorts.

Explainable Recommendation has attracted a lot of attention due to a renewed interest in explainable artificial intelligence. In particular, post-hoc approaches have proved to be the most easily applicable ones to increasingly complex recommendation models, which are then treated as black-boxes. The most recent literature has shown that for post-hoc explanations based on local surrogate models, there are problems related to the robustness of the approach itself. This consideration becomes even more relevant in human-related tasks like recommendation. The explanation also has the arduous task of enhancing increasingly relevant aspects of user experience such as transparency or trustworthiness. This paper aims to show how the characteristics of a classical post-hoc model based on surrogates is strongly model-dependent and does not prove to be accountable for the explanations generated., Comment: accepted at KaRS Workshop @RecSys 2021

The treatment of C6 glioma cells with the nitric oxide donor, PAPANONOate ((Z)-[N-(3-ammoniopropyl)-N-(n-propyl)amino]diazen-1-ium-1,2-diolate), resulted in a dose-dependent inhibition of cell proliferation. This was associated to a rapid and significant increase of ceramide levels and was mimicked by treatments that augment cellular ceramide. Metabolic experiments with radioactive sphingosine, serine, and choline showed that nitric oxide strongly reduced the utilization of ceramide for the biosynthesis of both sphingomyelin and glucosylceramide. Nevertheless, nitric oxide did not modify the activity of different enzymes of ceramide metabolism. The possibility that nitric oxide impairs the availability of ceramide for sphingolipid biosynthesis was then investigated. The metabolism of N-hexanoyl-[(3)H]sphingosine demonstrated that nitric oxide did not affect the biosynthesis of N-hexanoyl-[(3)H]sphingolipids but inhibited the metabolic utilization of long chain [(3)H]ceramide, synthesized in the endoplasmic reticulum (ER) from the recycled [(3)H]sphingosine. Moreover, results obtained with fluorescent ceramides, brefeldin A, ATP depletion, as well as in a ceramide transport assay indicate that nitric oxide impairs the traffic of ceramide from ER to Golgi apparatus. All this supports that, in glioma cells, the modulation of ceramide traffic can contribute to the regulation of its intracellular levels and participate in the nitric oxide-activated signaling pathway involved in the control of cell proliferation.

Aiming to investigate the possible production of ceramide-1-phosphate from complex sphingolipid metabolism in neurons, we administered radiolabeled sphingolipids to cerebellar granule cells and inspected the formation of labeled ceramide-1-phosphate in different experimental conditions. We report that differentiated granule cells are capable to form Cer-1-P via ceramide derived from SM degradation at the plasma membrane level. Moreover we observed that ceramide-1-phosphate can be also produced from a metabolic pathway not involving SM degradation. In particular, we obtained evidence that ceramide, synthesized via the recycling of sphingosine produced from ganglioside catabolism, can also be the precursor of ceramide-1-phosphate. We also found that undifferentiated and differentiated granule cells display different capacities to phosphorylate Cer produced by the two different metabolic pathways. The results here obtained demonstrate that cerebellar neurons are able to metabolically produce ceramide-1-phosphate and support that this molecule may serve a potential role in sphingoid-mediated signaling in the nervous system.

This is the preface for the joint workshop between KaRS and ComplexRec: two workshops co-located with the 15th ACM RecSys 2021 conference.

The objective is to reconstruct the subchondral bone after curettage of benign tumors located in the epiphysis, a relevant topic in oncological orthopedics. Several bones substituted are commercially available, yet none of these are suitably moldable to repair or be placed in the bone defect; although autologous bone for little defects and homologous for bigger defects are still considered the standard in reconstruction, we verify the ability to adapt and support articular cartilage through the application of Plexur M (Registered Trademark), a newly engineered biomaterial bone. In the present study, we enrolled the first ten consecutive cases referred to our department, where patients were affected by a benign epiphyseal tumor destroying the subchondral bone through to the articular cartilage. Every patient underwent curettage of the disease, apposition of a newly engineered biomaterial bone and filling with homologous morselized bone. The quality of reconstruction was evaluated by two surgeons and by a radiologist based on the achievement of surgical objectives and comparing pre and postoperative imaging. In seven out of eight cases of lesions located in the lower limbs the quality of reconstruction was considered good, restoring an adequate support to the articular cartilage. The quality of the remaining case was considered poor probably due to the extent of the spread of the disease, which destroyed the entire proximal tibial epiphysis. In the two cases where the disease was located in the upper limbs, the Plexur M application restored support to the articular cartilage sufficiently well. However, in the case of a giant cell tumor of the distal radial epiphysis there was a slight reabsorption of the morselized homologous bone. Our series suggest that Plexur M should be considered a valid option for orthopedic surgeons in restoring adequate mechanical support to the articular cartilage; nevertheless, considering its high cost, its use might be reserved to selected cases until further studies can verify the integration process, the effects on the survival of the articular cartilage and on the prevention of premature osteoarthritis.