Soluble low-density lipoprotein receptor-related protein 1 as a surrogate marker of carotid plaque inflammation assessed by 18F-FDG PET in patients with a recent ischemic stroke.

BACKGROUND: 18F-fluorodeoxyglucose positron emission tomography (18F-FDG PET) identifies carotid plaque inflammation and predicts stroke recurrence. AIM: Our aim was to evaluate the performance of soluble low-density lipoprotein receptor-related protein 1 (sLRP1) as an indicator of carotid plaque inflammation. METHODS: A prospective study was conducted among adult patients with recent (< 7 days) anterior circulation ischemic stroke and at least one atherosclerotic plaque in the ipsilateral internal carotid artery. Patients underwent an early (< 15 days from inclusion) 18F-FDG PET, and the maximum standardized uptake value (SUVmax) within the plaque was measured. sLRP1 levels were measured in plasma samples by ELISA. The association of sLRP1 with SUVmax was assessed using bivariate and multivariable linear regression analyses. Hazard ratios (HR) were estimated with Cox regression to evaluate the association between circulating sLRP1 and stroke recurrence. RESULTS: The study was conducted with 64 participants, of which 57.8% had ≥ 50% carotid stenosis. The multivariable linear and logistic regression analyses showed that sLRP1 was independently associated with (i) SUVmax within the plaque (ß = 0.159, 95% CI 0.062-0.257, p = 0.002) and (ii) a probability of presenting SUVmax ≥ 2.85 g/mL (OR = 1.31, 95% CI 1.00-1.01, p = 0.046), respectively. Participants with stroke recurrence showed higher sLRP1 levels at baseline [6447 ng/mL (4897-11163) vs. 3713 ng/mL (2793-4730); p = 0.018]. CONCLUSIONS: sLRP1 was independently associated with carotid plaque inflammation as measured by 18F-FDG PET in patients with recent ischemic stroke and carotid atherosclerosis.

Special Issue: New Insight into the Molecular Role of Lipids and Lipoproteins in Vascular Diseases.

Lipids and lipoproteins play a key role in cardiovascular diseases (CVD), mainly in the development of atherosclerosis [...].

Can Electronegative LDL Act as a Multienzymatic Complex?

Electronegative LDL (LDL(-)) is a minor form of LDL present in blood for which proportions are increased in pathologies with increased cardiovascular risk. In vitro studies have shown that LDL(-) presents pro-atherogenic properties, including a high susceptibility to aggregation, the ability to induce inflammation and apoptosis, and increased binding to arterial proteoglycans; however, it also shows some anti-atherogenic properties, which suggest a role in controlling the atherosclerotic process. One of the distinctive features of LDL(-) is that it has enzymatic activities with the ability to degrade different lipids. For example, LDL(-) transports platelet-activating factor acetylhydrolase (PAF-AH), which degrades oxidized phospholipids. In addition, two other enzymatic activities are exhibited by LDL(-). The first is type C phospholipase activity, which degrades both lysophosphatidylcholine (LysoPLC-like activity) and sphingomyelin (SMase-like activity). The second is ceramidase activity (CDase-like). Based on the complementarity of the products and substrates of these different activities, this review speculates on the possibility that LDL(-) may act as a sort of multienzymatic complex in which these enzymatic activities exert a concerted action. We hypothesize that LysoPLC/SMase and CDase activities could be generated by conformational changes in apoB-100 and that both activities occur in proximity to PAF-AH, making it feasible to discern a coordinated action among them.

Novel Therapeutic Approaches to Prevent Atherothrombotic Ischemic Stroke in Patients with Carotid Atherosclerosis.

Atherothrombotic stroke represents approximately 20% of all ischemic strokes. It is caused by large-artery atherosclerosis, mostly in the internal carotid artery, and it is associated with a high risk of early recurrence. After an ischemic stroke, tissue plasminogen activator is used in clinical practice, although it is not possible in all patients. In severe clinical situations, such as high carotid stenosis (≥70%), revascularization by carotid endarterectomy or by stent placement is carried out to avoid recurrences. In stroke prevention, the pharmacological recommendations are based on antithrombotic, lipid-lowering, and antihypertensive therapy. Inflammation is a promising target in stroke prevention, particularly in ischemic strokes associated with atherosclerosis. However, the use of anti-inflammatory strategies has been scarcely studied. No clinical trials are clearly successful and most preclinical studies are focused on protection after a stroke. The present review describes novel therapies addressed to counteract inflammation in the prevention of the first-ever or recurrent stroke. The putative clinical use of broad-spectrum and specific anti-inflammatory drugs, such as monoclonal antibodies and microRNAs (miRNAs) as regulators of atherosclerosis, will be outlined. Further studies are necessary to ascertain which patients may benefit from anti-inflammatory agents and how.

Epigenetic Regulation by microRNAs in Hyperhomocysteinemia-Accelerated Atherosclerosis.

Increased serum levels of homocysteine (Hcy) is a risk factor for cardiovascular disease and is specifically linked to various diseases of the vasculature such as atherosclerosis. However, the precise mechanisms by which Hcy contributes to this condition remain elusive. During the development of atherosclerosis, epigenetic modifications influence gene expression. As such, epigenetic modifications are an adaptive response to endogenous and exogenous factors that lead to altered gene expression by methylation and acetylation reactions of different substrates and the action of noncoding RNA including microRNAs (miRNAs). Epigenetic remodeling modulates cell biology in both physiological and physiopathological conditions. DNA and histone modification have been identified to have a crucial role in the progression of atherosclerosis. However, the potential role of miRNAs in hyperHcy (HHcy)-related atherosclerosis disease remains poorly explored and might be essential as well. There is no review available yet summarizing the contribution of miRNAs to hyperhomocystein-mediated atherogenicity or their potential as therapeutic targets even though their important role has been described in numerous studies. Specifically, downregulation of miR-143 or miR-125b has been shown to regulate VSCMs proliferation in vitro. In preclinical studies, downregulation of miR-92 or miR195-3p has been shown to increase the accumulation of cholesterol in foam cells and increase macrophage inflammation and atherosclerotic plaque formation, respectively. Another preclinical study found that there is a reciprocal regulation between miR-148a/152 and DNMT1 in Hcy-accelerated atherosclerosis. Interestingly, a couple of studies have shown that miR-143 or miR-217 may be used as potential biomarkers in patients with HHcy that may develop atherosclerosis. Moreover, the current review will also update current knowledge on miRNA-based therapies, their challenges, and approaches to deal with Hcy-induced atherosclerosis.

Presence of Ceramidase Activity in Electronegative LDL.

Electronegative low-density lipoprotein (LDL(-)) is a minor modified fraction of human plasma LDL with several atherogenic properties. Among them is increased bioactive lipid mediator content, such as lysophosphatidylcholine (LPC), non-esterified fatty acids (NEFA), ceramide (Cer), and sphingosine (Sph), which are related to the presence of some phospholipolytic activities, including platelet-activating factor acetylhydrolase (PAF-AH), phospholipase C (PLC), and sphingomyelinase (SMase), in LDL(-). However, these enzymes' activities do not explain the increased Sph content, which typically derives from Cer degradation. In the present study, we analyzed the putative presence of ceramidase (CDase) activity, which could explain the increased Sph content. Thin layer chromatography (TLC) and lipidomic analysis showed that Cer, Sph, and NEFA spontaneously increased in LDL(-) incubated alone at 37 °C, in contrast with native LDL(+). An inhibitor of neutral CDase prevented the formation of Sph and, in turn, increased Cer content in LDL(-). In addition, LDL(-) efficiently degraded fluorescently labeled Cer (NBD-Cer) to form Sph and NEFA. These observations defend the existence of the CDase-like activity's association with LDL(-). However, neither the proteomic analysis nor the Western blot detected the presence of an enzyme with known CDase activity. Further studies are thus warranted to define the origin of the CDase-like activity detected in LDL(-).

Information and communication technologies in neonatal health.

OBJECTIVES: To identify scientific evidence on the use and results of information and communication technologies for the improvement of neonatal health in general or specific health problems or interventions, and to describe the type of intervention and its results. METHODS: A systematic review of the available evidence was performed. The search was carried out in peer-reviewed journals between January 1, 2008 and April 30, 2018, in English and Spanish. The searched key terms were (health informatics OR telemedicine OR mHealth) AND (newborn OR newborn care OR neonatal care). RESULTS: From a total of 305 articles initially identified, 10 articles fulfilled the inclusion criteria. The main domains of eHealth identified as applied to neonatal health were telemedicine (3 studies), eLearning (1 study) and mHealth (7 studies). Target population were health care providers or parents. The studies aimed at diagnosis, provision of health care and training, promoting adherence to interventions in parents or improving quality of care. CONCLUSIONS: The use of eHealth in general and specifically focused on neonatal health shows important possibilities for development and expansion, given the advances and present needs, and should be considered a key tool for the reduction of inequalities.

OBJETIVOS: Identificar la evidencia científica sobre el uso y los resultados de las tecnologías de la información y la comunicación para mejorar la salud neonatal en general o problemas de salud o intervenciones específicos, y describir el tipo de intervención y sus resultados. MÉTODOS: Se realizó una revisión sistemática de la evidencia disponible. La búsqueda se llevó a cabo en revistas revisadas por pares entre el 1 de enero de 2008 y el 30 de abril de 2018, en español e inglés. Los términos clave de la búsqueda fueron (health informatics OR telemedicine OR mHealth) AND (newborn OR newborn care OR neonatal care). RESULTADOS: De un total de 305 artículos identificados inicialmente, 10 artículos cumplieron los criterios de inclusión. Los principales dominios de la eSalud aplicados a la salud neonatal fueron la telemedicina (3 estudios), el aprendizaje electrónico (1 estudio) y la salud móvil (7 estudios). La población destinataria consistió en los proveedores de atención de la salud o los padres. Los estudios tenían por objeto el diagnóstico, la prestación de atención sanitaria y la capacitación, la promoción del cumplimiento de las intervenciones en los padres o la mejora de la calidad de la atención. CONCLUSIONES: El uso de la eSalud en general, y específicamente en la salud neonatal, muestra importantes posibilidades de desarrollo y expansión, dados los avances y las necesidades actuales, y debería considerarse un instrumento clave para la reducción de las desigualdades.

Search for Reliable Circulating Biomarkers to Predict Carotid Plaque Vulnerability.

Atherosclerosis is responsible for 20% of ischemic strokes, and the plaques from the internal carotid artery the most frequently involved. Lipoproteins play a key role in carotid atherosclerosis since lipid accumulation contributes to plaque progression and chronic inflammation, both factors leading to plaque vulnerability. Carotid revascularization to prevent future vascular events is reasonable in some patients with high-grade carotid stenosis. However, the degree of stenosis alone is not sufficient to decide upon the best clinical management in some situations. In this context, it is essential to further characterize plaque vulnerability, according to specific characteristics (lipid-rich core, fibrous cap thinning, intraplaque hemorrhage). Although these features can be partly detected by imaging techniques, identifying carotid plaque vulnerability is still challenging. Therefore, the study of circulating biomarkers could provide adjunctive criteria to predict the risk of atherothrombotic stroke. In this regard, several molecules have been found altered, but reliable biomarkers have not been clearly established yet. The current review discusses the concept of vulnerable carotid plaque, and collects existing information about putative circulating biomarkers, being particularly focused on lipid-related and inflammatory molecules.

Inflammatory intracellular pathways activated by electronegative LDL in monocytes.

AIMS: Electronegative LDL (LDL(-)) is a plasma LDL subfraction that induces cytokine release in monocytes through toll-like receptor 4 (TLR4) activation. However, the intracellular pathways induced by LDL(-) downstream TLR4 activation are unknown. We aimed to identify the pathways activated by LDL(-) leading to cytokine release in monocytes. METHODS AND RESULTS: We determined LDL(-)-induced activation of several intracellular kinases in protein extracts from monocytes using a multikinase ELISA array. LDL(-) induced higher p38 mitogen-activated protein kinase (MAPK) phosphorylation than native LDL. This was corroborated by a specific cell-based assay and it was dependent on TLR4 and phosphoinositide 3-kinase (PI3k)/Akt pathway. P38 MAPK activation was involved in cytokine release promoted by LDL(-). A specific ELISA showed that LDL(-) activated cAMP response-element binding (CREB) in a p38 MAPK dependent manner. P38 MAPK was also involved in the nuclear factor kappa-B (NF-kB) and activating protein-1 (AP-1) activation by LDL(-). We found that NF-kB, AP-1 and CREB inhibitors decreased LDL(-)-induced cytokine release, mainly on MCP1, IL6 and IL10 release, respectively. CONCLUSIONS: LDL(-) promotes p38 MAPK phosphorylation through TLR4 and PI3k/Akt pathways. Phosphorylation of p38 MAPK is involved in NF-kB, AP-1 and CREB activation, leading to LDL(-)-induced cytokine release in monocytes.

Hypoxia induces metalloproteinase-9 activation and human vascular smooth muscle cell migration through low-density lipoprotein receptor-related protein 1-mediated Pyk2 phosphorylation.

OBJECTIVE: Hypoxia disturbs vascular function by promoting extracellular matrix remodeling. Extracellular matrix integrity and composition are modulated by metalloproteinases (MMPs). Our aim was to investigate the role of low-density lipoprotein receptor-related protein 1 (LRP1) in regulating MMP-9/MMP-2 activation and vascular smooth muscle cells (VSMCs) migration in response to hypoxia, and to elucidate the LRP1-signaling pathways involved in this process. APPROACH AND RESULTS: Western blot analysis showed that hypoxia induced a sustained phosphorylation of proline-rich tyrosine kinase 2 concomitantly with LRP1 overexpression in human VSMCs (hVSMCs). Deletion of LRP1 using small-interfering RNA technology or treatment of hVSMCs with the Src family kinase inhibitor PP2 impaired hypoxia-induced phosphorylation of proline-rich tyrosine kinase 2 levels. Coimmunoprecipitation experiments showed that the higher amounts of phosphorylation of proline-rich tyrosine kinase 2/LRP1ß immunoprecipitates in hypoxic hVSMCs were abolished in PP2-treated hVSMCs. Both LRP1 silencing and PP2 treatment were highly effective in the prevention of hypoxia-induced MMP-9 activation and hVSMC migration. Cellular subfractionation experiments revealed that PP2 effects may be caused by impairment of hypoxia-induced nuclear factor-κß translocation to the nucleus. ELISA measurements showed that LRP1 silencing but not PP2 treatment increased interleukin-1ß, interleukin-6, and monocyte chemoattractant protein-1 secretion by hypoxic hVSMCs. CONCLUSIONS: Our findings determine a crucial role of LRP1-mediated Pyk2 phosphorylation on hypoxia-induced MMP-9 activation and hVSMC migration and therefore in hypoxia-induced vascular remodeling. Both LRP1 silencing and PP2 treatments also influence hypoxia-induced proinflammatory effects in hVSMCs. Therefore, further studies are required to establish therapeutical strategies that efficiently modulate vascular remodeling and inflammation associated with hypoxia-vascular diseases.

Development of an ASR System for Medical Conversations.

In this work we document the development of an ASR system for the transcription of conversations between patient and doctor and we will point out the critical aspects of the domain. The system was trained with an acoustic base of spontaneous speech that has a domain language model and a supervised phonetic dictionary. Its performance was compared with two systems: a) NeMo End-to-End Conformers in Spanish and b) Google API ASR (Automatic Speech Recognition) Cloud. The evaluation was carried out on a set of 208 teleconsultations recorded during the year 2020. The WER (Word Error Rate) was evaluated in ASR, and Recall and F1 for recognized medical entities. In conclusion, the developed system performed better, reaching 72.5% accuracy in the domain of teleconsultations and an F1 for entity recognition of 0.80.

Automatic Speech Recognition System to Record Progress Notes in a Mobile EHR: A Pilot Study.

Creating notes in the EHR is one of the most problematic aspects for health professionals. The main challenges are the time spent on this task and the quality of the records. Automatic speech recognition technologies aim to facilitate clinical documentation for users, optimizing their workflow. In our hospital, we internally developed an automatic speech recognition system (ASR) to record progress notes in a mobile EHR. The objective of this article is to describe the pilot study carried out to evaluate the implementation of ASR to record progress notes in a mobile EHR application. As a result, the specialty that used ASR the most was Home Medicine. The lack of access to a computer at the time of care and the need to perform short and fast evolutions were the main reasons for users to use the system.

PCSK9 plasma concentration is associated with epicardial adipose tissue volume and metabolic control in patients with type 1 diabetes.

Patients with type 1 diabetes (T1D) have a greater risk of cardiovascular disease. Proconvertase subtilisin-kexin 9 (PCSK9) is involved in the atherosclerosis process. This study aimed to determine the relationship between PCSK9 levels and epicardial adipose tissue (EAT) volume and cardiometabolic variables in patients with T1D. This was an observational cross-sectional study including 73 patients with T1D. Clinical, biochemical and imaging data were collected. We divided the patients into two groups according to their glycemic control and the EAT index (iEAT) percentile. We performed a correlation analysis between the collected variables and PCSK9 levels; subsequently, we performed a multiple regression analysis with the significant parameters. The mean age was 47.6 ± 8.5 years, 58.9% were men, and the BMI was 26.9 ± 4.6 kg/m2. A total of 31.5%, 49.3% and 34.2% of patients had hypertension, dyslipidemia and smoking habit, respectively. The PCSK9 concentration was 0.37 ± 0.12 mg/L, which was greater in patients with worse glycemic control (HbA1c > 7.5%), dyslipidemia and high EAT volume (iEAT > 75th percentile). The PCSK9 concentration was positively correlated with age (r = 0.259; p = 0.027), HbA1c (r = 0.300; p = 0.011), insulin dose (r = 0.275; p = 0.020), VLDL-C level (r = 0.331; p = 0.004), TG level (r = 0.328; p = 0.005), and iEAT (r = 0.438; p < 0.001). Multiple regression analysis revealed that 25% of the PCSK9 variability was explained by iEAT and HbA1c (p < 0.05). The PCSK9 concentration is associated with metabolic syndrome parameters, poor glycemic control and increased EAT volume in patients with T1D.

Artificial Intelligence Assistance for the Measurement of Full Alignment Parameters in Whole-Spine Lateral Radiographs.

BACKGROUND: Measuring spinal alignment with radiological parameters is essential in patients with spinal conditions likely to be treated surgically. These evaluations are not usually included in the radiological report. As a result, spinal surgeons commonly perform the measurement, which is time-consuming and subject to errors. We aim to develop a fully automated artificial intelligence (AI) tool to assist in measuring alignment parameters in whole-spine lateral radiograph (WSL X-rays). METHODS: We developed a tool called Vertebrai that automatically calculates the global spinal parameters (GSPs): Pelvic incidence, sacral slope, pelvic tilt, L1-L4 angle, L4-S1 lumbo-pelvic angle, T1 pelvic angle, sagittal vertical axis, cervical lordosis, C1-C2 lordosis, lumbar lordosis, mid-thoracic kyphosis, proximal thoracic kyphosis, global thoracic kyphosis, T1 slope, C2-C7 plummet, spino-sacral angle, C7 tilt, global tilt, spinopelvic tilt, and hip odontoid axis. We assessed human-AI interaction instead of AI performance alone. We compared the time to measure GSP and inter-rater agreement with and without AI assistance. Two institutional datasets were created with 2267 multilabel images for classification and 784 WSL X-rays with reference standard landmark labeled by spinal surgeons. RESULTS: Vertebrai significantly reduced the measurement time comparing spine surgeons with AI assistance and the AI algorithm alone, without human intervention (3 minutes vs. 0.26 minutes; P < 0.05). Vertebrai achieved an average accuracy of 83% in detecting abnormal alignment values, with the sacral slope parameter exhibiting the lowest accuracy at 61.5% and spinopelvic tilt demonstrating the highest accuracy at 100%. Intraclass correlation analysis revealed a high level of correlation and consistency in the global alignment parameters. CONCLUSIONS: Vertebrai's measurements can accurately detect alignment parameters, making it a promising tool for measuring GSP automatically.

Bioinformatics Architecture for Integrating Genomics Data into Electronic Health Records.

The adequate management of patients' genomic information is essential for any health institution pursuing the Precision Medicine model. Here we approach a bioinformatic architecture that allows the Institution to store its whole genetic test data in a scalable database, and also the integration of that genetic data with the Electronic Health Record through a Clinical Decision Support System. The system complements patient care by suggesting referral to genetic counseling for patients who are potentially at risk of hereditary breast/ovarian cancer, and allowing for proper follow-up of patients with pathogenic variants in BRCA1 or BRCA2 genes. The implemented solution uses the FHIR standard and genetic nomenclatures from the Human Genome Variation Society and the HUGO Gene Nomenclature Committee. The architecture is flexible enough to allow any other health institution to integrate -to their information ecosystem- the whole solution or some of the modules according to its degree of digitization progress.

Apolipoprotein J protects cardiomyocytes from lipid-mediated inflammation and cytotoxicity induced by the epicardial adipose tissue of diabetic patients.

Diabetic patients present increased volume and functional alterations in epicardial adipose tissue (EAT). We aimed to analyze EAT from type 2 diabetic patients and the inflammatory and cytotoxic effects induced on cardiomyocytes. Furthermore, we analyzed the cardioprotective role of apolipoprotein J (apoJ). EAT explants were obtained from nondiabetic patients (ND), diabetic patients without coronary disease (DM), and DM patients with coronary disease (DM-C) after heart surgery. Morphological characteristics and gene expression were evaluated. Explants were cultured for 24 h and the content of nonesterified fatty acids (NEFA) and sphingolipid species in secretomes was evaluated by lipidomic analysis. Afterwards, secretomes were added to AC16 human cardiomyocytes for 24 h in the presence or absence of cardioprotective molecules (apoJ and HDL). Cytokine release and apoptosis/necrosis were assessed by ELISA and flow cytometry. The EAT from the diabetic samples showed altered expression of genes related to lipid accumulation, insulin resistance, and inflammation. The secretomes from the DM samples presented an increased ratio of pro/antiatherogenic ceramide (Cer) species, while those from DM-C contained the highest concentration of saturated NEFA. DM and DM-C secretomes promoted inflammation and cytotoxicity on AC16 cardiomyocytes. Exogenous Cer16:0, Cer24:1, and palmitic acid reproduced deleterious effects in AC16 cells. These effects were attenuated by exogenous apoJ. Diabetic secretomes promoted inflammation and cytotoxicity in cardiomyocytes. This effect was exacerbated in the secretomes of the DM-C samples. The increased content of specific NEFA and ceramide species seems to play a key role in inducing such deleterious effects, which are attenuated by apoJ.

Integrating Dermoscopic Images into PACS Using DICOM and Modality Worklist.

Dermatology is one of the medical fields outside the radiology service that uses image acquisition and analysis in its daily medical practice, mostly through digital dermoscopy imaging modality. The acquisition, transfer, and storage of dermatology images has become an important issue to resolve. We aimed to describe our experience in integrating dermoscopic images into PACS using DICOM as a guide for the health informatics and dermatology community. During 2022 we integrated the video dermoscopy equipment through a strategic plan with an 8-step procedure. We used the DICOM standard with Modality Worklist and Storage commitment. Three systems were involved (video dermoscopy software, the EHR, and PACS). We identified critical steps and faced many challenges, such as the lack of a final model of DICOM standard for dermatology images.

Electronegative LDL: a circulating modified LDL with a role in inflammation.

Electronegative low density lipoprotein (LDL(-)) is a minor modified fraction of LDL found in blood. It comprises a heterogeneous population of LDL particles modified by various mechanisms sharing as a common feature increased electronegativity. Modification by oxidation is one of these mechanisms. LDL(-) has inflammatory properties similar to those of oxidized LDL (oxLDL), such as inflammatory cytokine release in leukocytes and endothelial cells. However, in contrast with oxLDL, LDL(-) also has some anti-inflammatory effects on cultured cells. The inflammatory and anti-inflammatory properties ascribed to LDL(-) suggest that it could have a dual biological effect.

The Induction of Cytokine Release in Monocytes by Electronegative Low-Density Lipoprotein (LDL) Is Related to Its Higher Ceramide Content than Native LDL.

Electronegative low-density lipoprotein (LDL(-)) is a minor modified LDL subfraction that is present in blood. LDL(-) promotes inflammation and is associated with the development of atherosclerosis. We previously reported that the increase of cytokine release promoted by this lipoprotein subfraction in monocytes is counteracted by high-density lipoprotein (HDL). HDL also inhibits a phospholipase C-like activity (PLC-like) intrinsic to LDL(-). The aim of this work was to assess whether the inhibition of the PLC-like activity by HDL could decrease the content of ceramide (CER) and diacylglycerol (DAG) generated in LDL(-). This knowledge would allow us to establish a relationship between these compounds and the inflammatory activity of LDL(-). LDL(-) incubated at 37 °C for 20 h increased its PLC-like activity and, subsequently, the amount of CER and DAG. We found that incubating LDL(-) with HDL decreased both products in LDL(-). Native LDL was modified by lipolysis with PLC or by incubation with CER-enriched or DAG-enriched liposomes. The increase of CER in native LDL significantly increased cytokine release, whereas the enrichment in DAG did not show these inflammatory properties. These data point to CER, a resultant product of the PLC-like activity, as a major determinant of the inflammatory activity induced by LDL(-) in monocytes.

A dataset of skin lesion images collected in Argentina for the evaluation of AI tools in this population.

In recent years, numerous dermatological image databases have been published to make possible the development and validation of artificial intelligence-based technologies to support healthcare professionals in the diagnosis of skin diseases. However, the generation of these datasets confined to certain countries as well as the lack of demographic information accompanying the images, prevents having a real knowledge of in which populations these models could be used. Consequently, this hinders the translation of the models to the clinical setting. This has led the scientific community to encourage the detailed and transparent reporting of the databases used for artificial intelligence developments, as well as to promote the formation of genuinely international databases that can be representative of the world population. Through this work, we seek to provide details of the processing stages of the first public database of dermoscopy and clinical images created in a hospital in Argentina. The dataset comprises 1,616 images corresponding to 1,246 unique lesions collected from 623 patients.