Diabetic kidney disease (DKD) is a frequently chronic kidney pathology derived from diabetes comorbidity. This condition has irreversible damage and its risk factor increases with SARS-CoV-2 infection. The prognostic outcome for diabetic patients with COVID-19 is dismal, even with intensive medical treatment. However, there is still scarce information on critical genes involved in the pathophysiological impact of COVID-19 on DKD. Herein, we characterize differential expression gene (DEG) profiles and determine hub genes undergoing transcriptional reprogramming in both disease conditions. Out of 995 DEGs, we identified 42 shared with COVID-19 pathways. Enrichment analysis elucidated that they are significantly induced with implications for immune and inflammatory responses. By performing a protein–protein interaction (PPI) network and applying topological methods, we determine the following five hub genes: STAT1, IRF7, ISG15, MX1 and OAS1. Then, by network deconvolution, we determine their co-expressed gene modules. Moreover, we validate the conservancy of their upregulation using the Coronascape database (DB). Finally, tissue-specific regulation of the five predictive hub genes indicates that OAS1 and MX1 expression levels are lower in healthy kidney tissue. Altogether, our results suggest that these genes could play an essential role in developing severe outcomes of COVID-19 in DKD patients.

Background: Currently, there is clear evidence that apoptosis plays an important role in the development and progression of tumors. One of the best characterized apoptosis triggering systems is the CD95/Fas/APO-1 pathway; previous reports have demonstrated high levels of soluble CD95 (sCD95) in serum of patients with some types of cancer. Cervical cancer is the second most common cancer among women worldwide. As a first step in an attempt to design a minimally invasive test to predict the risk of developing cervical cancer in patients with precancerous lesions, we used a simple assay based on the capacity of human serum to induce apoptosis in Jurkat cells. We evaluated the relationship between sCD95 levels and the ability to induce apoptosis in Jurkat cells in cervical cancer patients and controls.

The CD95 pathway is a critical apoptotic pathway used by immune cells to avoid cancer development. CD95 ligand (CD95L) is found in several forms, as a cell membrane-associated form, a soluble metalloprotease-cleaved form, and a soluble but membrane-bound CD95L released on cell-derived exosomes. In this study, we used a cell-based assay to evaluate the activity of proapoptotic CD95L in sera from healthy individuals and breast cancer patients. We confirmed that our cell-based assay using Jurkat cells was sensitive to the presence of proapoptotic CD95L in serum, and apoptosis induction by mechanisms other than CD95 was discriminated using apoptosis-resistant Jurkat subclones. Our results indicated a proapoptotic potential of normal serum that involved CD95L. Sera from breast cancer patients exhibited significantly decreased apoptosis induction, due to increased CD95 receptor levels compared with healthy women. Apoptotic potential tended to decrease as the Breast Imaging Reporting and Data System grade increased, and we observed restoration of proapoptotic potential after tumor removal. The CD95L in serum responsible for apoptotic induction was associated with high-molecular-weight particles, perhaps with exosomes. The sera of healthy individuals generally contain a proapoptotic environment, and this property is mainly maintained by the presence of CD95L. Furthermore, measurement of CD95L-mediated apoptosis induction by sera could be a useful parameter to be evaluated during cancer development and therapeutic response.

En los últimos años, se ha deforestado el 20% de manglar a nivel mundial. México es de los países con mayor pérdida de superficie de mangle, algo que contribuye a las emisiones de CO2 e impulsa el cambio climático. Sin embargo, falta conocimiento sobre los factores que influyen en la pérdida y la ganancia del manglar, las emisiones de CO2, y la dinámica de usos de suelo y cobertura vegetal a escala local y regional. Por tanto, los objetivos de este estudio fueron analizar la dinámica de uso de suelo en la zona de Marismas Nacionales (México) durante el periodo 1981–2015, determinar la tasa de deforestación y degradación anual del manglar y estimar las emisiones de CO2 derivadas de estos procesos utilizando técnicas de información geográfica. Para determinar los cambios de uso de suelo, con la matriz de tabulación cruzada, se adquirieron diversos parámetros de cambio que permitieron generar una ecuación para estimar la tasa de deforestación y degradación. Con los datos del Inventario Nacional de Emisiones de Gases y Compuestos de Efecto Invernadero (México), se estimaron las emisiones y las absorciones de CO2 (equivalente, CO2e) promovidas por deforestación, degradación, reforestación y recuperación natural de manglares. Para el periodo 1981–2005, la emisión estimada fue de 432.50 Gg de CO2e debido a una tasa anual de deforestación del 0.77%, y la degradación fue de 27.16 Gg de CO2e a una tasa anual de1 7.64%. Para el periodo 2005–2015, la emisión fue de 145.21 Gg de CO2e debido a una tasa anual de deforestación del 0.44%, y la degradación fue de 24.80 Gg de CO2e a una tasa anual del 4.94%. La mayor pérdida de manglar se debió a la transformación a suelos con categorías de agrícola-pecuario y desarrollo antrópico. La degradación sucedió por fenómenos naturales y actividades antropogénicas.