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Respiratory diseases and cardiovascular diseases (CVDs) have high prevalence and share common risk factors. In some respiratory diseases such as sleep apnoea and COPD, the evidence of their negative impact on the prognosis of CVDs seems clear. However, in other diseases it is less evident whether there is any direct relationship. With this in mind, our objective was to provide information that may be helpful to better understand the relationship between respiratory pathology and CVDs.There are different reasons for this relationship, such as shared risk factors, common pathophysiological mechanisms, side effects of treatment and the direct effect in the heart and great vessels of respiratory diseases.Indeed, aging and smoking are risk factors for CVDs and also for respiratory diseases such as obstructive sleep apnea (OSA), COPD and interstitial lung diseases (ILD).Furthermore, there are common pathophysiological mechanisms that affect both respiratory diseases and CVDs, such as accelerated atherosclerosis, microvascular dysfunction, endothelial dysfunction, inflammation, hypoxemia and oxidative stress.Besides that, it is well known that lung cancer, sarcoidosis and amyloidosis may directly affect the heart and great vessels.Finally, side effects of drugs for respiratory diseases and the discontinuation of treatments that are necessary for CVDs, such as β-blockers and aspirin, may have a deleterious impact on the cardiovascular system.In conclusion, the coexistence of respiratory diseases and CVDs is very common. It makes modifying diagnostic and therapeutic management necessary and is also a relevant prognostic factor. Resumen: Las enfermedades respiratorias y cardiovasculares (ECVs) tienen una alta prevalencia y comparten factores de riesgo comunes. En algunas enfermedades respiratorias como la apnea del sueño y la EPOC, la evidencia de su impacto negativo en el pronóstico de las ECVs parece clara. Sin embargo, en otras enfermedades es menos evidente si existe alguna relación directa. Considerando esto, nuestro objetivo fue aportar información que pueda ser útil para comprender mejor la relación entre la patología respiratoria y las ECVs.Existen diferentes razones para esta relación, como factores de riesgo compartidos, mecanismos fisiopatológicos comunes, efectos secundarios del tratamiento y el efecto directo en el corazón y los grandes vasos de las enfermedades respiratorias.De hecho, el envejecimiento y el tabaquismo son factores de riesgo para las ECVs y también para las enfermedades respiratorias como la apnea obstructiva del sueño (AOS), la EPOC y las enfermedades pulmonares intersticiales (EPID).Además, existen mecanismos fisiopatológicos comunes que afectan tanto a las enfermedades respiratorias como a las ECVs, como la aterosclerosis acelerada, la disfunción microvascular, la disfunción endotelial, la inflamación, la hipoxemia y el estrés oxidativo. Además, es bien conocido que el cáncer de pulmón, la sarcoidosis y la amiloidosis pueden afectar directamente al corazón y a los grandes vasos.Finalmente, los efectos secundarios de los fármacos para enfermedades respiratorias y la suspensión de tratamientos necesarios para las ECVs, como los β-bloqueantes y la aspirina, pueden tener un impacto deletéreo sobre el sistema cardiovascular.En conclusión, la coexistencia de enfermedades respiratorias y ECVs es muy frecuente, lo que obliga a modificar el manejo diagnóstico y terapéutico y es, además, un factor pronóstico relevante.

ABSTRACT: Objective: To analyse differences in clinical presentation and outcome between bacteraemic pneumococcal community-acquired pneumonia (B-PCAP) and sSvere Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) pneumonia. Methods: This observational multi-centre study was conducted on patients hospitalized with B-PCAP between 2000 and 2020 and SARS-CoV-2 pneumonia in 2020. Thirty-day survival, predictors of mortality, and intensive care unit (ICU) admission were compared. Results: In total, 663 patients with B-PCAP and 1561 patients with SARS-CoV-2 pneumonia were included in this study. Patients with B-PCAP had more severe disease, a higher ICU admission rate and more complications. Patients with SARS-CoV-2 pneumonia had higher in-hospital mortality (10.8% vs 6.8%; P=0.004). Among patients admitted to the ICU, the need for invasive mechanical ventilation (69.7% vs 36.2%; P

Summary: Upon tissue injury, cytokine expression reprogramming transiently remodels the inflammatory immune microenvironment to activate repair processes and subsequently return to homeostasis. However, chronic inflammation induces permanent changes in cytokine production which exacerbate tissue damage and may even favor tumor development. Here, we address the contribution of post-transcriptional regulation, by the RNA-binding protein CPEB4, to intestinal immune homeostasis and its role in inflammatory bowel diseases (IBD) and colorectal cancer (CRC) development. We found that intestinal damage induces CPEB4 expression in adaptive and innate immune cells, which is required for the translation of cytokine mRNA(s) such as the one encoding interleukin-22. Accordingly, CPEB4 is required for the development of gut-associated lymphoid tissues and to maintain intestinal immune homeostasis, mediating repair and remodeling after acute inflammatory tissue damage and promoting the resolution of intestinal inflammation. CPEB4 is chronically overexpressed in inflammatory cells in patients with IBD and in CRC, favoring tumor development.

Introduction: Postsurgical Lumbar facet joint syndrome (PLFJS) is a clinical entity characterized by acute or chronic lumbar pain which can irradiate to the lower extremities but never with a dermatomal pattern in postsurgical patients of lumbar surgery. The diagnosis and treatment are with a Diagnostic Facet Block (DFB). This study describes the outcome of patients undergoing DFB after lumbar surgery and compares the results with patients without surgery. Methods: An analytic and longitudinal study with patients over 18 years old between January 2018 and January 2020. For the comparative analysis, we performed two groups: non-surgical lumbar facet joint syndrome (NSLFJS) and PLFJS. Results: The general prevalence of PLFJS in our population was 12.5%. The results after DBF showed a significant decrease in the Oswestry percentage and pain according to the Visual Analog Scale(VAS) for the NSLFJS and PLFJS groups between the 3 surgical stages (pre-DFB, post-DFB at 6 weeks and post-DFB at 6 months), but no significant differences between the 2 groups. Discussion: The VAS and Oswestry reported a significant improvement in both groups of patients. The innervation of the lumbar facet joints causes pain, this is secondary to the pathological neural activity of facet arthritis that arises because of chronic postsurgical inflammation or chronic degenerative changes. Conclusion: The origin of the LFJS is the arthrosis of the facet, originated by postsurgical or degenerative changes. DFB is effectivefor decreasing pain of facet joint origin in patients with previous lumbar surgery.

Background: DNA methylation (DNAm) may contribute to processes that underlie associations between air pollution and poor health. Therefore, our objective was to evaluate associations between DNAm and ambient concentrations of particulate matter (PM) ≤2.5, ≤10, and 2.5–10 μm in diameter (PM2.5; PM10; PM2.5–10). Methods: We conducted a methylome-wide association study among twelve cohort- and race/ethnicity-stratified subpopulations from the Women's Health Initiative and the Atherosclerosis Risk in Communities study (n = 8397; mean age: 61.5 years; 83% female; 45% African American; 9% Hispanic/Latino American). We averaged geocoded address-specific estimates of daily and monthly mean PM concentrations over 2, 7, 28, and 365 days and 1 and 12 months before exams at which we measured leukocyte DNAm in whole blood. We estimated subpopulation-specific, DNAm-PM associations at approximately 485,000 Cytosine-phosphate-Guanine (CpG) sites in multi-level, linear, mixed-effects models. We combined subpopulation- and site-specific estimates in fixed-effects, inverse variance-weighted meta-analyses, then for associations that exceeded methylome-wide significance and were not heterogeneous across subpopulations (P 0.10), we characterized associations using publicly accessible genomic databases and attempted replication in the Cooperative Health Research in the Region of Augsburg (KORA) study. Results: Analyses identified significant DNAm-PM associations at three CpG sites. Twenty-eight-day mean PM10 was positively associated with DNAm at cg19004594 (chromosome 20; MATN4; P = 3.33 × 10−8). One-month mean PM10 and PM2.5–10 were positively associated with DNAm at cg24102420 (chromosome 10; ARPP21; P = 5.84 × 10−8) and inversely associated with DNAm at cg12124767 (chromosome 7; CFTR; P = 9.86 × 10−8). The PM-sensitive CpG sites mapped to neurological, pulmonary, endocrine, and cardiovascular disease-related genes, but DNAm at those sites was not associated with gene expression in blood cells and did not replicate in KORA. Conclusions: Ambient PM concentrations were associated with DNAm at genomic regions potentially related to poor health among racially, ethnically and environmentally diverse populations of U.S. women and men. Further investigation is warranted to uncover mechanisms through which PM-induced epigenomic changes may cause disease. Keywords: Particulate matter, DNA methylation, Epigenetics, Air pollution, Epigenome-wide association study