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<title>02.02. Área de Salud II Cartagena</title>
<link href="https://sms.carm.es/ricsmur/handle/123456789/17144" rel="alternate"/>
<subtitle/>
<id>https://sms.carm.es/ricsmur/handle/123456789/17144</id>
<updated>2026-08-17T10:15:08Z</updated>
<dc:date>2026-08-17T10:15:08Z</dc:date>
<entry>
<title>Management of pneumonia by the emergency radiologist</title>
<link href="https://sms.carm.es/ricsmur/handle/123456789/27276" rel="alternate"/>
<author>
<name>Plasencia-Martínez, Juana-María</name>
</author>
<author>
<name>Bravo-Urbieta, Joaquín</name>
</author>
<author>
<name>Blanco-Barrio, Ana</name>
</author>
<id>https://sms.carm.es/ricsmur/handle/123456789/27276</id>
<updated>2026-08-03T10:48:11Z</updated>
<published>2026-12-01T00:00:00Z</published>
<summary type="text">Management of pneumonia by the emergency radiologist
Plasencia-Martínez, Juana-María; Bravo-Urbieta, Joaquín; Blanco-Barrio, Ana
Susceptibility to pulmonary infection depends not only on the patient's clinical condition but also on the characteristics of the microorganism, such as its virulence and transmissibility, which are influenced by environmental factors, antimicrobial resistance patterns, and the emergence of pandemics. Understanding these factors, together with the patterns of pulmonary dissemination and their radiological appearances, helps narrow the differential diagnosis. In the emergency setting, however, the radiologist's role extends beyond suggesting the aetiology of pneumonia. Recognition of potential complications, guidance on treatment implications, and assessment of prognosis are key contributions. This paper illustrates these concepts through a literature review and real clinical cases.
</summary>
<dc:date>2026-12-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>Assessment of diabetes self-management education guideline content across Spanish regions: a document-based comparative analysis.</title>
<link href="https://sms.carm.es/ricsmur/handle/123456789/27275" rel="alternate"/>
<author>
<name>Moore, James-Richard</name>
</author>
<author>
<name>Roldán-Chicano, María-Teresa</name>
</author>
<author>
<name>Cebrián-Cuenca, Ana-María</name>
</author>
<author>
<name>Esteban-Flores, Ana</name>
</author>
<id>https://sms.carm.es/ricsmur/handle/123456789/27275</id>
<updated>2026-08-03T10:48:12Z</updated>
<published>2026-07-01T00:00:00Z</published>
<summary type="text">Assessment of diabetes self-management education guideline content across Spanish regions: a document-based comparative analysis.
Moore, James-Richard; Roldán-Chicano, María-Teresa; Cebrián-Cuenca, Ana-María; Esteban-Flores, Ana
OBJECTIVE: This study aims to evaluate the content, structure, and alignment with international standards of Diabetes Self-Management Education guidelines across Spain's regional healthcare systems. It focuses on comparing the guidelines and documents used in these programs against international standards to identify key patterns, disparities, and areas for improvement. METHODS: The study employed a comparative descriptive analysis, systematically reviewing and contrasting 13 relevant documents from the Spanish Ministry of Health and regional health authorities. The evaluation was based on international standards for DSME, set by the American Diabetes Association and the Global Diabetes Survey. Key aspects assessed included program structure, target population, content delivery, healthcare provider involvement, and quality management. RESULTS: The results revealed significant variability in the DSME guidelines, with most emphasising individualised education and a multidisciplinary approach. However, there were gaps in addressing psychosocial factors, dietary support and the inclusion of vulnerable populations. Additionally, quality management and evaluation processes were inconsistently described, with some regional guidelines lacking systematic assessment frameworks. CONCLUSION: The study highlights the need for harmonising DSME guidelines across Spain. It recommends improving inclusivity, psychosocial support, multidisciplinary involvement, quality monitoring, and digital delivery to strengthen diabetes education and reduce regional inequalities nationwide.
</summary>
<dc:date>2026-07-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>Non-decameric NLRP3 reveals a TGN/MTOC-distal pathway of inflammasome activation</title>
<link href="https://sms.carm.es/ricsmur/handle/123456789/27227" rel="alternate"/>
<author>
<name>Mateo-Tortola, María</name>
</author>
<author>
<name>Hochheiser, Inga-V</name>
</author>
<author>
<name>Li, Gaopeng</name>
</author>
<author>
<name>Funk, Lukas</name>
</author>
<author>
<name>Hashemi, Atousa</name>
</author>
<author>
<name>Liu, Xiao</name>
</author>
<author>
<name>Torp, Jane</name>
</author>
<author>
<name>Erlebach, Lena</name>
</author>
<author>
<name>Szolek, Andras</name>
</author>
<author>
<name>Grga, Jelena</name>
</author>
<author>
<name>Bork, Francesca</name>
</author>
<author>
<name>Muller, Jana-S</name>
</author>
<author>
<name>Kronenberg-Versteeg, Deborah</name>
</author>
<author>
<name>Geyer, Matthias</name>
</author>
<author>
<name>Weber, Alexander-N-R</name>
</author>
<author>
<name>Tapia-Abellán, Ana</name>
</author>
<id>https://sms.carm.es/ricsmur/handle/123456789/27227</id>
<updated>2026-08-03T10:48:13Z</updated>
<published>2026-05-30T00:00:00Z</published>
<summary type="text">Non-decameric NLRP3 reveals a TGN/MTOC-distal pathway of inflammasome activation
Mateo-Tortola, María; Hochheiser, Inga-V; Li, Gaopeng; Funk, Lukas; Hashemi, Atousa; Liu, Xiao; Torp, Jane; Erlebach, Lena; Szolek, Andras; Grga, Jelena; Bork, Francesca; Muller, Jana-S; Kronenberg-Versteeg, Deborah; Geyer, Matthias; Weber, Alexander-N-R; Tapia-Abellán, Ana
The NLRP3 inflammasome contributes to a wide range of conditions from infections to Alzheimer's disease. NLRP3 forms an inactive decameric cage, that upon interaction with the trans-Golgi network (TGN) and microtubule organization center (MTOC), leads to inflammasome activation, yet whether non-decamer NLRP3 species form functional inflammasomes remains unclear. Here, we design a NLRP3 exon 3 deletion variant that forms low molecular weight NLRP3 assemblies. Spatially and dynamically highly resolved microscopy in THP-1 and human macrophages shows that nigericin, a K(+)-dependent NLRP3 stimulus, can trigger two distinct activation pathways: (i) the rapidly engaged decameric cage-dependent pathway; and (ii) a decameric cage-independent, TGN/MTOC-distal, and slow-reacting pathway employed by low molecular weight NLRP3 species, that dominates in human neutrophils. Collectively, our results delineate two parallel yet biologically distinct NLRP3 activation pathways, thereby providing a framework to understand NLRP3-driven inflammation across a wide range of pathological context and cell types.
</summary>
<dc:date>2026-05-30T00:00:00Z</dc:date>
</entry>
<entry>
<title>Identification of new overlapping and disease-specific genetic risk factors for rheumatoid arthritis and radiographic axial spondyloarthritis: a meta-analysis of three large European populations and functional characterization</title>
<link href="https://sms.carm.es/ricsmur/handle/123456789/27212" rel="alternate"/>
<author>
<name>Cabrera-Serrano, Antonio-José</name>
</author>
<author>
<name>Carretero-Fernández, María</name>
</author>
<author>
<name>Pérez-Rojo, Begoña</name>
</author>
<author>
<name>ter-Horst, Rob</name>
</author>
<author>
<name>Caadas-Garre, Marisa</name>
</author>
<author>
<name>Canhao, Helena</name>
</author>
<author>
<name>Quartuccio, Luca</name>
</author>
<author>
<name>Sorensen, Signe-B</name>
</author>
<author>
<name>Glintborg, Bente</name>
</author>
<author>
<name>Filipescu, Ileana</name>
</author>
<author>
<name>Pérez-Pampin, Eva</name>
</author>
<author>
<name>Conesa-Zamora, Pablo</name>
</author>
<author>
<name>Swierkot, Jerzy</name>
</author>
<author>
<name>den-Broeder, Alfons-A</name>
</author>
<author>
<name>de-Vita, Salvatore</name>
</author>
<author>
<name>Brix-Petersen, Eva-Rabing</name>
</author>
<author>
<name>Li, Yang</name>
</author>
<author>
<name>Coenen, Marieke-J-H</name>
</author>
<author>
<name>Bogunia-Kubik, Katarzyna</name>
</author>
<author>
<name>Andersen, Vibeke</name>
</author>
<author>
<name>Fonseca, Joao-Eurico</name>
</author>
<author>
<name>Lund-Hetland, Merete</name>
</author>
<author>
<name>López-Nevot, Miguel-Ángel</name>
</author>
<author>
<name>López-Medina, Clementina</name>
</author>
<author>
<name>Reyes-Zurita, Fernando-Jesus</name>
</author>
<author>
<name>Netea, Mihai-G</name>
</author>
<author>
<name>Escudero, Alejandro</name>
</author>
<author>
<name>Caliz, Rafael</name>
</author>
<author>
<name>Collantes-Estévez, Eduardo</name>
</author>
<author>
<name>Sánchez-Maldonado, José-Manuel</name>
</author>
<author>
<name>Sainz, Juan</name>
</author>
<id>https://sms.carm.es/ricsmur/handle/123456789/27212</id>
<updated>2026-08-03T10:48:59Z</updated>
<published>2026-04-23T00:00:00Z</published>
<summary type="text">Identification of new overlapping and disease-specific genetic risk factors for rheumatoid arthritis and radiographic axial spondyloarthritis: a meta-analysis of three large European populations and functional characterization
Cabrera-Serrano, Antonio-José; Carretero-Fernández, María; Pérez-Rojo, Begoña; ter-Horst, Rob; Caadas-Garre, Marisa; Canhao, Helena; Quartuccio, Luca; Sorensen, Signe-B; Glintborg, Bente; Filipescu, Ileana; Pérez-Pampin, Eva; Conesa-Zamora, Pablo; Swierkot, Jerzy; den-Broeder, Alfons-A; de-Vita, Salvatore; Brix-Petersen, Eva-Rabing; Li, Yang; Coenen, Marieke-J-H; Bogunia-Kubik, Katarzyna; Andersen, Vibeke; Fonseca, Joao-Eurico; Lund-Hetland, Merete; López-Nevot, Miguel-Ángel; López-Medina, Clementina; Reyes-Zurita, Fernando-Jesus; Netea, Mihai-G; Escudero, Alejandro; Caliz, Rafael; Collantes-Estévez, Eduardo; Sánchez-Maldonado, José-Manuel; Sainz, Juan
INTRODUCTION: This study conducted a meta-analysis across three large European cohorts (UKBB, FinnGen, and REPAIR), including 12,660 rheumatoid arthritis (RA) cases, 2,446 radiographic axial spondyloarthritis (r-axSpA) cases, and over 530,000 shared controls. METHODS: Ten independent SNPs in CARMIL1, GRM4, ITPR3, PRSS16, ZNF322, HTT, IKZF1, MANEA, and MGAM2 were analyzed, and functional characterization was performed through cytokine and protein assessments as well as eQTL analyses. RESULTS: Ten independent SNPs were significantly associated with both RA and r-axSpA. Risk alleles included HTT (rs363075A), IKZF1 (rs12718261A), MANEA (rs72920280T), and MGAM2 (rs73158426G), while CARMIL1 (rs72831267C), GRM4 (rs2495964G), ITPR3 (rs77601296A), ITPR3 (rs9469540T), PRSS16 (rs72843633T), and ZNF322 (rs6901425G) had protective effects. Functional analysis showed that GRM4 (rs2495964G) was linked to decreased CCL25 levels (p = 0.00030), and ITPR3 (rs9469540T) to reduced IL10 production after LPS stimulation (p = 1.3×10(-4)). The ZNF322rs6901425G allele was associated with reduced TNFB and increased TGM2 levels (p = 9.60×10(-4) and p = 3.00×(10-4)), both involved in immune signaling and tissue remodeling. Disease-specific associations were found in BTN2A1, BTN3A2, and H2BC11. The BTN2A1 (rs1977199A) allele was protective in RA (OR = 0.93) but increased r-axSpA risk (OR = 1.23), and was associated with reduced IL22 (p = 0.00016) and elevated HO-1 in obese individuals (p = 6.73×10(-6)). In contrast, BTN3A2 (rs9393716G) and H2BC11 (rs66462181C) increased RA risk but were protective in r-axSpA, linked to decreased HO-1 and IL6 (p = 2.43×10(-5), 3.287times;10(-4), 1.18×10(-4)). These SNPs also acted as eQTLs for immune-related genes such as BTN3A2, HMGN4, and TRIM38. DISCUSSION: Our findings highlight novel shared and disease-specific variants and key immunoregulatory mediators-IL10, IL22, IL6, CCL25, and HO-1-offering insights for disease stratification and therapeutic targeting.
</summary>
<dc:date>2026-04-23T00:00:00Z</dc:date>
</entry>
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