Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for the current coronavirus disease 2019 (COVID-19) pandemic, affecting more than 219 countries and causing the death of ...more than 5 million people worldwide. The genetic background represents a factor that predisposes the way the host responds to SARS-CoV-2 infection. In this sense, genetic variants of
and
could explain the observed interindividual variability to COVID-19 outcomes. In order to improve the understanding of how genetic variants of
and
are involved in the severity of COVID-19, we included a total of 481 individuals who showed clinical manifestations of COVID-19 and were diagnosed by reverse transcription PCR (RT-PCR). Genomic DNA was extracted from peripheral blood and saliva samples.
insertion/deletion polymorphism was evaluated by the high-resolution melting method;
single-nucleotide polymorphism (SNP) (rs4344) and
SNPs (rs2285666 and rs2074192) were genotyped using TaqMan probes. We assessed the association of ACE and ACE2 polymorphisms with disease severity using logistic regression analysis adjusted by age, sex, hypertension, type 2 diabetes, and obesity. The severity of the illness in our study population was divided as 31% mild, 26% severe, and 43% critical illness; additionally, 18% of individuals died, of whom 54% were male. Our results showed in the codominant model a contribution of
gene rs2285666 T/T genotype to critical outcome odds ratio (OR) = 1.83; 95%CI = 1.01-3.29; p = 0.04 and to require oxygen supplementation (OR = 1.76; 95%CI = 1.01-3.04; p = 0.04), in addition to a strong association of the T allele of this variant to develop critical illness in male individuals (OR = 1.81; 95%CI = 1.10-2.98; p = 0.02). We suggest that the T allele of rs2285666 represents a risk factor for severe and critical outcomes of COVID-19, especially for men, regardless of age, hypertension, obesity, and type 2 diabetes.
Serine proteases play a critical role during SARS-CoV-2 infection. Therefore, polymorphisms of transmembrane protease serine 2 (
) and serpine family E member 1 (
) could help to elucidate the ...contribution of variability to COVID-19 outcomes.
To evaluate the genetic variants of the genes previously associated with COVID-19 outcomes, we performed a cross-sectional study in which 1536 SARS-CoV-2-positive participants were enrolled.
(rs2070788, rs75603675, rs12329760) and
(rs2227631, rs2227667, rs2070682, rs2227692) were genotyped using the Open Array Platform. The association of polymorphisms with disease outcomes was determined by logistic regression analysis adjusted for covariates (age, sex, hypertension, type 2 diabetes, and obesity).
According to our codominant model, the GA genotype of rs2227667 (OR=0.55; 95% CI = 0.36-0.84;
=0.006) and the AG genotype of rs2227667 (OR=0.59; 95% CI = 0.38-0.91;
=0.02) of
played a protective role against disease. However, the rs2227692 T allele and TT genotype
(OR=1.45; 95% CI = 1.11-1.91;
=0.006; OR=2.08; 95% CI = 1.22-3.57;
=0.007; respectively) were associated with a decreased risk of death. Similarly, the rs75603675 AA genotype
had an OR of 1.97 (95% CI = 1.07-3.6;
=0.03) for deceased patients. Finally, the rs2227692 T allele
was associated with increased D-dimer levels (OR=1.24; 95% CI = 1.03-1.48;
=0.02).
Our data suggest that the rs75603675
and rs2227692
polymorphisms are associated with a poor outcome. Additionally, rs2227692
could participate in hypercoagulable conditions in critical COVID-19 patients, and this genetic variant could contribute to the identification of new pharmacological targets and treatment strategies to block the inhibition of TMPRSS2 entry into SARS-CoV-2.
During a viral infection, the immune response is mediated by the toll-like receptors and myeloid differentiation Factor 88 (MyD88) that play an important role sensing infections such as SARS-CoV-2 ...which has claimed the lives of more than 6.8 million people around the world.
We carried out a cross-sectional with a population of 618 SARS-CoV-2-positive unvaccinated subjects and further classified based on severity: 22% were mild, 34% were severe, 26% were critical, and 18% were deceased. Toll Like Receptor 7 (TLR7) single-nucleotide polymorphisms (rs3853839, rs179008, rs179009, and rs2302267) and MyD88 (rs7744) were genotyped using TaqMan OpenArray. The association of polymorphisms with disease outcomes was performed by logistic regression analysis adjusted by covariates.
A significant association of rs3853839 and rs7744 of the TLR7 and MyD88 genes, respectively, was found with COVID-19 severity. The G/G genotype of the rs3853839 TLR7 was associated with the critical outcome showing an Odd Ratio = 1.98 (95% IC = 1.04–3.77). The results highlighted an association of the G allele of MyD88 gene with severe, critical and deceased outcomes. Furthermore, in the dominant model (AG + GG vs. AA), we observed an Odd Ratio = 1.70 (95% CI = 1.02–2.86) with severe, Odd Ratio = 1.82 (95% CI = 1.04–3.21) with critical, and Odd Ratio = 2.44 (95% CI = 1.21–4.9) with deceased outcomes.
To our knowledge this work represents an innovative report that highlights the significant association of TLR7 and MyD88 gene polymorphisms with COVID-19 outcomes and the possible implication of the MyD88 variant with D-dimer and IFN-α concentrations.
Display adaptation in nomadic environments Niño-Tavera, Luis Carlos; Carrillo-Ramos, Angela; Ruiz, Edgar Enrique
Proceedings of the 7th International Conference on Advances in Mobile Computing and Multimedia,
12/2009
Conference Proceeding
NOMAD, acronym of NOmadic Model for display ADaptation oriented to final users is a model that improves the adaptation of the information in any device that face consults from many different ...Information Sources (IS) and the characteristics of the Ubiquitous Computation making the interaction process between the user and his context. Oriented to final users, the NOMAD model has as a principle the personalization through the user preferences considering the display and allows embracing the device physical characteristics that restrict the different ways to present the information, through the personal computing paradigm. Also, it established a standard for capturing the restrictions in a session with the purpose of presenting services in a ubiquitous environment, estimating its functionality under a set of scenarios that evidence its validity and performance. NOMAD makes easier the scalability of components for the enrichment of the characteristics that impact the information display based on ontologies that define a particular session.
To characterize CD4
+
CD28
null
cells in chronic hyperuricemia and investigate whether allopurinol could restore CD28 expression and the balance of T helper phenotypes. Asymptomatic individuals with ...chronic hyperuricemia and ultrasonographic findings evocative of urate deposition in the joints. Age- and gender-matched normouricemic individuals were also studied. Oral allopurinol at 150 mg/day for 4 weeks, followed by 300 mg/day through week 12. Color-flow cytometry on peripheral blood mononuclear cells (PBMC) with antibodies against CD4, CD28, T-bet (Th1), GATA-3 (Th2), and RORγt (Th17). Six patients (five men, median age of 53 years) and seven controls were studied. At baseline, hyperuricemic patients had more CD4
+
CD28
null
/CD4
+
cells than normouricemic subjects (36.8% vs. 6.1%;
p
= 0.001), with a predominance of T-bet
+
cells (98.5% vs. 6.6%;
p
= 0.001) and few RORγt
+
cells (0.7% vs. 89.4%;
p
= 0.014). In hyperuricemic patients, the number of CD4
+
cells/10,000 PBMC was similar before and after allopurinol (3378 vs. 3954;
p
= 0.843). Conversely, CD4
+
CD28
null
cells decreased from 36.8% (23.0–43.7) to 15.8% (4.7–28.1;
p
= 0.031). CD4
+
CD28
null
T-bet
+
cells decreased from 98.5% (95.0–99.4) to 88.3% (75.2–98.9;
p
= 0.062), CD4
+
CD28
null
GATA-3
+
cells increased from 0% (0–4.0) to 2.8% (0.1–15.6;
p
= 0.156), and CD4
+
CD28
null
RORγt
+
cells increased from 0.7% (0.4–7.0) to 4.5% (1.3–28.1;
p
= 0.031). The CD4
+
CD28
null
cell subset is abnormally expanded in chronic hyperuricemia, despite the absence of overt urate-related disease. Allopurinol may partially restore CD28 expression on CD4
+
cells while enhancing the homeostatic balance of T helper phenotypes. ClinicalTrials.gov, number NCT04012294.
Key Points
• Chronic hyperuricemia is characterized by an abnormal expansion of senescent CD4
+
CD28
null
cells, which are aberrantly polarized toward a Th1 effector phenotype.
• Allopurinol administration restores CD28 expression on CD4
+
cells while enhancing the homeostatic balance of helper T phenotypes.
To characterize CD4
CD28
cells in chronic hyperuricemia and investigate whether allopurinol could restore CD28 expression and the balance of T helper phenotypes. Asymptomatic individuals with chronic ...hyperuricemia and ultrasonographic findings evocative of urate deposition in the joints. Age- and gender-matched normouricemic individuals were also studied. Oral allopurinol at 150 mg/day for 4 weeks, followed by 300 mg/day through week 12. Color-flow cytometry on peripheral blood mononuclear cells (PBMC) with antibodies against CD4, CD28, T-bet (Th1), GATA-3 (Th2), and RORγt (Th17). Six patients (five men, median age of 53 years) and seven controls were studied. At baseline, hyperuricemic patients had more CD4
CD28
/CD4
cells than normouricemic subjects (36.8% vs. 6.1%; p = 0.001), with a predominance of T-bet
cells (98.5% vs. 6.6%; p = 0.001) and few RORγt
cells (0.7% vs. 89.4%; p = 0.014). In hyperuricemic patients, the number of CD4
cells/10,000 PBMC was similar before and after allopurinol (3378 vs. 3954; p = 0.843). Conversely, CD4
CD28
cells decreased from 36.8% (23.0-43.7) to 15.8% (4.7-28.1; p = 0.031). CD4
CD28
T-bet
cells decreased from 98.5% (95.0-99.4) to 88.3% (75.2-98.9; p = 0.062), CD4
CD28
GATA-3
cells increased from 0% (0-4.0) to 2.8% (0.1-15.6; p = 0.156), and CD4
CD28
RORγt
cells increased from 0.7% (0.4-7.0) to 4.5% (1.3-28.1; p = 0.031). The CD4
CD28
cell subset is abnormally expanded in chronic hyperuricemia, despite the absence of overt urate-related disease. Allopurinol may partially restore CD28 expression on CD4
cells while enhancing the homeostatic balance of T helper phenotypes. ClinicalTrials.gov, number NCT04012294.
La acuicultura cuenta con sistemas de monitoreo de calidad del agua tradicionales, que recurren al control de los parámetros fisicoquímicos de forma manual, por esta razón se desarrolló e implementó ...una plataforma de monitoreo automático en tiempo real, la cual permite el análisis remoto de variables fisicoquímicas en criaderos de tilapias. Este sistema utiliza sensores de temperatura, pH, oxígeno disuelto y turbidez, que están conectados a microcontroladores encargados del procesamiento de datos y la transmisión a través de redes (LPWAN). Estos datos son transmitidos a través de modulación de radiofrecuencia LoRa, y están interconectados con un Gateway, que funciona como un enlace entre el nodo final y la infraestructura de red convencional basada en TCP/IP, para retransmitirla empleando el protocolo MQTT a un Bróker, alojado en un (VPS), de tal forma que la información se presenta mediante una interfaz de usuario basada en Web, los datos son visualizados en un dashboard, con la opción de acceder a tablas y gráficos de registro históricos de los parámetros monitoreados. Este método permite que criaderos ubicados en zonas rurales lejanas, con un acceso limitado de ancho de banda a internet, puedan contar con un sistema de monitoreo en tiempo real.
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