Correction of Tropical Rainfall Measuring Missions Satellite Data of Solar Radiation for the High Andean Areas of Peru

The spatial and temporal quantification of climatic elements is necessary in different regions of the world, as mitigation policies against climate change in recent years the use of renewable energies has been promoted, with solar radiation being an important element, the objective is to correct Tropical Rainfall Measuring Missions (TRMM) satellite data series of solar radiation with respect to the data observed through an automatic meteorological station for a short period at a point located in the southern Peruvian Andes, we proceeded to process the observed data and download satellite information, making use of From a mathematical model, the correction coefficients of the satellite data were determined; The multiplicative factor model better corrects the satellite information, the Pearson correlation improved from R = 0.65 to R = 0.84 for monthly solar radiation, in the series of satellite data corrected for 37 years, a trend was determined -0.0006 Watt/m2/month

Pseudo-Four Component Synthesis of Mono- and Di-Benzylated-1,2,3-Triazoles Derived from Aniline

The pseudo-four component click synthesis of dibenzylated 1,2,3-triazoles derived from aniline is reported. The cycloaddition of sodium azide to N-(prop-2-ynyl)-benzenamine (I) in the presence of equimolar amounts of p-substituted benzyl derivatives, yields a mixture of mono- and dibenzylated 1,2,3-triazoles. When two equivalents of the benzyl derivative are added to the multicomponent reaction, the selective preparation of the dibenzylated compounds is achieved. The reactivity of the aniline N-H bond in monobenzylated 1,2,3-triazoles was tested by treatment with one equivalent of a p-substituted benzyl chloride at 40 °C, rendering the dibenzylated derivatives quantitatively

Urbanismo - AR284 - 202102

Descripción: El curso de Urbanismo realiza una reflexión sobre las Ciudades del Siglo 21 las cuales concentran una mayor población y actividades urbanas que las que albergaron las ciudades de siglos pasados. Las ciudades son el resultado de la aglomeración de personas, ante lo cual el reto es lograr una ciudad con calidad humana: inclusiva, resiliente, segura, medio ambientalmente responsable y sostenible. Este curso te introduce al conocimiento de la estructura y morfología de la ciudad: la compleja dinámica que generamos las personas al interactuar económica y socialmente en sus espacios, cómo percibimos estos espacios, cómo afectamos el medio ambiente y cómo el arquitecto configura los espacios de una ciudad sea una calle, una plaza o algún acogedor rincón de la ciudad con el diseño de sus edificaciones. Propósito: El curso ha sido diseñado con el propósito de permitir al futuro arquitecto desarrollar su capacidad de análisis, a través de la identificación de los diferentes aspectos que estructuran la dinámica de una ciudad, y el empleo de herramientas metodológicas para aplicarlas en el ejercicio profesional. El curso contribuye directamente al desarrollo de la competencia general de Ciudadanía y la competencia específica Gestión Profesional (que corresponde a los criterios NAAB : PC6 y SC2) ambas a un nivel intermedio (nivel 2). Tiene como requisito que el estudiante haya aprobado 100 créditos

Urbanismo - AR284 - 202101

Descripción: El curso de Urbanismo realiza una reflexión sobre las Ciudades del Siglo 21 las cuales concentran una mayor población y actividades urbanas que las que albergaron las ciudades de siglos pasados. Las ciudades son el resultado de la aglomeración de personas, ante lo cual el reto es lograr una ciudad con calidad humana: inclusiva, resiliente, segura, medio ambientalmente responsable y sostenible. Este curso te introduce al conocimiento de la estructura y morfología de la ciudad: la compleja dinámica que generamos las personas al interactuar económica y socialmente en sus espacios, cómo percibimos estos espacios, cómo afectamos el medio ambiente y cómo el arquitecto configura los espacios de una ciudad sea una calle, una plaza o algún acogedor rincón de la ciudad con el diseño de sus edificaciones. Propósito: El curso ha sido diseñado con el propósito de permitir al futuro arquitecto desarrollar su capacidad de análisis, a través de la identificación de los diferentes aspectos que estructuran la dinámica de una ciudad, y el empleo de herramientas metodológicas para aplicarlas en el ejercicio profesional. El curso contribuye directamente al desarrollo de la competencia general de Ciudadanía y la competencia específica Gestión Profesional (que corresponde a los criterios NAAB : PC6 y SC2) ambas a un nivel intermedio (nivel 2). Tiene como requisito que el estudiante haya aprobado 100 créditos

Targeting ABL-IRE1α Signaling Spares ER-Stressed Pancreatic β Cells to Reverse Autoimmune Diabetes.

(Cell Metabolism 25, 883–897; April 4, 2017) In the originally published version of this article, the immunoblot image of the HDAC1 nuclear extract protein control in Figure 3I was incorrectly cropped such that it included one extraneous lane. The corrected and original versions of Figure 3I are shown here. Furthermore, in the Discussion, after the sentence “Such compensatory, dysregulated UPR effects may be general as Perk deletion, likewise, hyperactivates IRE1α in β cells, which suffer early apoptosis, leading to postnatal diabetes,” we incorrectly cited Harding, H.P., and Ron, D. (2002). Endoplasmic reticulum stress and the development of diabetes: a review. Diabetes 51, S455–S461. The correct citation is: Harding, H.P., Zeng, H., Zhang, Y., Jungries, R., Chung, P., Plesken, H., Sabatini, D.D., and Ron, D. (2001). Diabetes mellitus and exocrine pancreatic dysfunction in perk−/− mice reveals a role for translational control in secretory cell survival. Molecular Cell 7, 1153–1163. The authors apologize for any confusion these errors may have caused. [Figure presented

Targeting ABL-IRE1α Signaling Spares ER-Stressed Pancreatic β Cells to Reverse Autoimmune Diabetes.

In cells experiencing unrelieved endoplasmic reticulum (ER) stress, the ER transmembrane kinase/endoribonuclease (RNase)-IRE1α-endonucleolytically degrades ER-localized mRNAs to promote apoptosis. Here we find that the ABL family of tyrosine kinases rheostatically enhances IRE1α's enzymatic activities, thereby potentiating ER stress-induced apoptosis. During ER stress, cytosolic ABL kinases localize to the ER membrane, where they bind, scaffold, and hyperactivate IRE1α's RNase. Imatinib-an anti-cancer tyrosine kinase inhibitor-antagonizes the ABL-IRE1α interaction, blunts IRE1α RNase hyperactivity, reduces pancreatic β cell apoptosis, and reverses type 1 diabetes (T1D) in the non-obese diabetic (NOD) mouse model. A mono-selective kinase inhibitor that allosterically attenuates IRE1α's RNase-KIRA8-also efficaciously reverses established diabetes in NOD mice by sparing β cells and preserving their physiological function. Our data support a model wherein ER-stressed β cells contribute to their own demise during T1D pathogenesis and implicate the ABL-IRE1α axis as a drug target for the treatment of an autoimmune disease

Regulatory T-cell Depletion Alters the Tumor Microenvironment and Accelerates Pancreatic Carcinogenesis

Regulatory T cells (Treg) are abundant in human and mouse pancreatic cancer. To understand the contribution to the immunosuppressive microenvironment, we depleted Tregs in a mouse model of pancreatic cancer. Contrary to our expectations, Treg depletion failed to relieve immunosuppression and led to accelerated tumor progression. We show that Tregs are a key source of TGFβ ligands and, accordingly, their depletion reprogramed the fibroblast population, with loss of tumor-restraining, smooth muscle actin-expressing fibroblasts. Conversely, we observed an increase in chemokines Ccl3, Ccl6, and Ccl8 leading to increased myeloid cell recruitment, restoration of immune suppression, and promotion of carcinogenesis, an effect that was inhibited by blockade of the common CCL3/6/8 receptor CCR1. Further, Treg depletion unleashed pathologic CD4+ T-cell responses. Our data point to new mechanisms regulating fibroblast differentiation in pancreatic cancer and support the notion that fibroblasts are a heterogeneous population with different and opposing functions in pancreatic carcinogenesis. SIGNIFICANCE: Here, we describe an unexpected cross-talk between Tregs and fibroblasts in pancreatic cancer. Treg depletion resulted in differentiation of inflammatory fibroblast subsets, in turn driving infiltration of myeloid cells through CCR1, thus uncovering a potentially new therapeutic approach to relieve immunosuppression in pancreatic cancer.See related commentary by Aykut et al., p. 345.This article is highlighted in the In This Issue feature, p. 327