Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), the causative agent of COVID-19, spread rapidly across the globe in 2020, with most countries experiencing two distinct waves of infection. In Brazil, the second wave was marked by the emergence of the P.1 (Gamma) variant, which disproportionately affected younger individuals and was associated with increased mortality. This study aimed to evaluate the epidemiological profile and post mortem histopathological lung findings, correlate them with laboratory results, and compare the first and second waves of COVID-19. To investigate neutrophil extracellular traps (NETs), we performed immunohistochemistry for citrullinated histone H3 (cit-H3) and myeloperoxidase (MPO). Our cohort included patients who died in the intensive care unit (ICU) of a single center in southern Brazil. The study included 42 patients, 24 from the first wave and 18 from the second, who died between March 2020 and August 2021. Laboratory data included complete blood counts and D-dimer levels. Histopathological analyses were conducted using H&E-stained slides and reviewed independently by two blinded pathologists. MPO and cit-H3 immunohistochemistry were performed to evaluate NETs markers. All cases exhibited varying degrees of inflammation and diffuse alveolar damage (DAD), with frequent microvascular thrombi. Neutrophilic infiltration was significantly higher in the second wave. Additionally, cases with intense neutrophilic infiltration showed a stronger association with thrombosis. NETs were identified in 10 cases. No significant correlation was found between histopathological findings, NETs, and laboratory blood count results. The histopathological findings were consistent with those reported globally. The second wave of COVID-19 showed higher neutrophilic infiltrate in the lung tissue. Neutrophils play a key role in the inflammatory response and NET formation might indicate an increased risk of mortality. Further studies can consider NET-targeted therapies as potential strategies.

Objective: To analyze the role of genes and single nucleotide polymorphisms previously associated with preterm birth as possible new risk indicators in relation to preterm births in pregnant women participating in the Curitiba Maternal and Child Health Cohort (COOSMIC). Methods: From a cohort started in 2018, a selection of 77 pregnant women was carried out from a specific group. This group was divided into a preterm group, of babies born at 37 weeks, and a term group, of babies born at more than 37 weeks of gestation. In addition, considering data on the oral condition of the pregnant women, they categorized two groups (adequate and inadequate oral condition). Target SNP-type polymorphisms (WNT4 - rs56318008 C/T, rs12037376 G/A; EBF1 - rs2963463 T/A, rs2946171 T/G; EEFSEC - rs2955117 G/A, rs1108313 A/G; AGTR2 - rs5194 A/C, rs373 6556 A/T), previously associated with preterm parts, were genotyped through real-time PCR (Applied Biosystem®) using TaqMan® probes. Results: The variable gestation time (term and preterm) showed in preterm development the absence of the GG genotype in rs5194 (A/G - AGTR2 gene). Conjugated analysis within the original group focusing on oral condition (adequate or inconvenient) indicates the high frequency of the AA genotype of rs1108313 (G/A – EEFSEC), also associated with premature births. Conclusions: The wild G allele of rs1108313 (G/A) in the EEFSEC gene showed risk in preterm births, especially in those with poor oral health. This SNP and conventional oral conditions are crucial risk indicators for assessing vulnerability in pregnant women under SUS care.

Background/Objectives: Rhabdomyosarcoma (RMS), the most common pediatric soft tissue sarcoma, includes two main subtypes, embryonal (eRMS) and alveolar (aRMS), each with distinct molecular and clinical characteristics. Although cellular processes underlying RMS and differences between PAX3-FOXO1 fusion-positive and fusion-negative tumors are well known, the contribution of long noncoding RNAs (lncRNAs) remains poorly understood. Methods: Here, we reannotated publicly available microarray datasets to comprehensively profile lncRNA expression and reconstruct lncRNA–miRNA–mRNA regulatory networks in RMS. Results: We identified several lncRNAs with subtype-specific differential expression, including HOTAIR as a potential sponge for miR-206, DSCR8 for miR-885-5p, and PRKCQ-AS1 for miR-515-5p in eRMS. Database-supported interaction analyses identified putative regulatory relationships between these lncRNAs and cancer-related miRNAs and mRNAs. Validation using the St. Jude Cloud PeCan platform confirmed distinct lncRNA expression signatures across RMS subtypes and other pediatric solid tumors, supporting subtype-specific regulation. Conclusions: Our findings provide an updated characterization of the lncRNA landscape in RMS and identify candidate lncRNA–miRNA–mRNA regulatory networks that may contribute to disease biology. The proposed regulatory interactions are hypothesis-generating and require experimental validation. Overall, our findings provide a resource for future functional studies and support the investigation of lncRNAs as potential biomarkers and therapeutic targets in RMS.

COVID-19 severity is frequently linked to exacerbated inflammation, with the inflammasome pathway playing a key role in activating inflammatory interleukins. This observational post-mortem study evaluated the expression of inflammasome-associated molecules in patients who died from COVID-19 during the second wave. Minimally invasive autopsies were performed on patients from the first (n = 24) and second (n = 18) waves. Lung tissue samples underwent immunohistochemical staining for ACE-2, TLR-4, NF-κB, TNF-α, NOX4, NLRP3, ASC, CASPASE-1, IL-1β, IL-18, GSDMD, and CASPASE-9. Additionally, genetic polymorphisms within inflammasome-related genes were assessed via real-time polymerase chain reaction. Lung tissue expressions of TLR-4, NLRP3, and IL-18 were significantly higher in patients from the second wave compared to those from the first, with expression levels of 26.3 versus 12.1, 13.9 versus 6.4, and 25.6 versus 3.8, respectively. The A allele at rs4648090 of NFKB1 and the T allele at rs317155 of NOX4 were associated with increased corresponding protein expression by factors of 5.1 and 8.9, respectively. Notably, IL-18 demonstrated substantial immunological relevance, correlating strongly with elevated expression linked to these genetic variants in second wave cases. These findings suggest that the inflammasome pathway harbors biologically meaningful molecules implicated in severe COVID-19, meriting further investigation for their potential as diagnostic or therapeutic targets.