Prediction of Adverse Maternal Outcomes in Women with Early-Onset Preeclampsia with Severe Features in Mexico: Validation of the Full-PIERS Model.

Objective: Validate the full-PIERS model in predicting adverse maternal outcomes in women with early-onset preeclampsia with severe features in our population. Methods: Retrospective cohort study. We applied the full-PIERS model on 130 women with severe early-onset preeclampsia who were treated at a second-level hospital in Nuevo León, México. We validated the full-PIERS model in its ability to discriminate through the AUROC. Results: The full-PIERS model applied to the data obtained in our study had good discrimination, revealing an AUC of 0.718 (95% CI 0.515-0.921; P = 0.017). A cut-off of 7.95 was identified as the cut-off point with the best diagnostic performance, with the highest Youden index, presenting a sensitivity of 54.5% and specificity of 99.2% for the development of complications. Conclusion: The full-PIERS model can predict adverse maternal outcomes in women admitted to our hospital with severe early-onset preeclampsia within 48 hours of admission.

Case Report: Fatal Rickettsiosis in Pregnancy.

Rocky Mountain spotted fever (RMSF) is a tick-borne infection caused by Rickettsia rickettsii. We present a series of two cases of pregnant patients who showed up at the emergency room of a hospital in Nuevo León, Mexico. Both patients lived in environments where R. rickettsii is endemic and they presented with several days of symptoms, including fever. Both patients developed a rash and had stillbirths during their hospital stay. Treatment with doxycycline was delayed, with fatal results in both patients. Diagnosis of RMSF was confirmed via polymerase chain reaction assay postmortem. The need to link epidemiological clues with clinical data is critical in the diagnosis and early treatment of RMSF to prevent maternal deaths.

Monitoring of Thermal Comfort and Air Quality for Sustainable Energy Management inside Hospitals Based on Online Analytical Processing and the Internet of Things.

There is a need to ensure comfortable conditions for hospital staff and patients from the point of view of thermal comfort and air quality so that they do not affect their performance. We consider the need for hospital employees and patients to enjoy conditions of greater well-being during their stay. This is understood as a comfortable thermal sensation and adequate air quality, depending on the task they are performing. The contribution of this article is the formulation of the fundamentals of a system and platform for monitoring thermal comfort and Indoor Air Quality (IAQ) in hospitals, based on an Internet of Things platform composed of a low-cost sensor node network that is capable of measuring critical variables such as humidity, temperature, and Carbon Dioxide (CO2). As part of the platform, a multidimensional data model with an On-Line Analytical Processing (OLAP) approach is presented that offers query flexibility, data volume reduction, as well as a significant reduction in query response times. The experimental results confirm the suitability of the platform's data model, which facilitates operational and strategic decision making in complex hospitals.

Identification of a novel long non-coding RNA within RUNX1 intron 5.

BACKGROUND: RUNX1 gene, a master regulator of the hematopoietic process, participates in pathological conditions as a partner for several genes in chromosomal translocations. One of the most frequent chromosomal translocations found in acute myeloid leukemia patients is the t(8;21), in which RUNX1 and ETO genes recombine. In RUNX1 gene, the DNA double-strand breaks that originate the t(8;21) are generated in the intron 5, specifically within three regions designated as BCR1, BCR2, and BCR3. To date, what determines that these regions are more susceptible to DNA double-strand breaks is not completely clear. In this report, we characterized RUNX1 intron 5, by analyzing DNase-seq and ChIP-seq data, available in the ENCODE Project server, to evaluate DNaseI hypersensitivity and the presence of the epigenetic mark H3K4me3 in 124 and 51 cell types, respectively. RESULTS: Our results show that intron 5 exhibits an epigenetic mark distribution similar to known promoter regions. Moreover, using the online tool YAPP and available CAGE data from the ENCODE Project server, we identified several putative transcription start sites within intron 5 in regions BCR2 and BCR3. Finally, available EST data was analyzed, identifying a novel uncharacterized long non-coding RNA, which is expressed in hematopoietic cell lines as shown by RT-PCR. Our data suggests that the core promoter of the novel long non-coding RNA locates within the region BCR3. CONCLUSION: We identified a novel long non-coding RNA within RUNX1 intron 5, transcribed from a promoter located in the region BCR3, one of the chromosomal breakpoints of RUNX1 gene.

Transcriptional Auto-Regulation of RUNX1 P1 Promoter.

RUNX1 a member of the family of runt related transcription factors (RUNX), is essential for hematopoiesis. The expression of RUNX1 gene is controlled by two promoters; the distal P1 promoter and the proximal P2 promoter. Several isoforms of RUNX1 mRNA are generated through the use of both promoters and alternative splicing. These isoforms not only differs in their temporal expression pattern but also exhibit differences in tissue specificity. The RUNX1 isoforms derived from P2 are expressed in a variety of tissues, but expression of P1-derived isoform is restricted to cells of hematopoietic lineage. However, the control of hematopoietic-cell specific expression is poorly understood. Here we report regulation of P1-derived RUNX1 mRNA by RUNX1 protein. In silico analysis of P1 promoter revealed presence of two evolutionary conserved RUNX motifs, 0.6kb upstream of the transcription start site, and three RUNX motifs within 170bp of the 5'UTR. Transcriptional contribution of these RUNX motifs was studied in myeloid and T-cells. RUNX1 genomic fragment containing all sites show very low basal activity in both cell types. Mutation or deletion of RUNX motifs in the UTR enhances basal activity of the RUNX1 promoter. Chromatin immunoprecipitation revealed that RUNX1 protein is recruited to these sites. Overexpression of RUNX1 in non-hematopoietic cells results in a dose dependent activation of the RUNX1 P1 promoter. We also demonstrate that RUNX1 protein regulates transcription of endogenous RUNX1 mRNA in T-cell. Finally we show that SCL transcription factor is recruited to regions containing RUNX motifs in the promoter and the UTR and regulates activity of the RUNX1 P1 promoter in vitro. Thus, multiple lines of evidence show that RUNX1 protein regulates its own gene transcription.