Development of a solar radiation sensor system with pyranometer

<span>Solar energy is a result of the nuclear fusion process in the form of a series of thermonuclear events that occur in the Sun's core. Solar radiation has a significant impact on the lives of all living things on earth. The uses, as mentioned earlier, are when the solar radiation received requires a certain amount and vice versa. As a result, a more accurate instrument of solar radiation is required. A specific instrument is typically used to measure solar radiation parameters. There are four solar radiation parameters: diffusion radiation, global radiation, direct radiation, and solar radiation duration. Thus, it needs to use many devices to measure radiation data. The paper designs to measure all four-radiation data by pyranometer with particular modification and shading device. This design results have a high correlation with a global standard with a value of R=0.73, diffusion with a value of R=0.60 and a sufficiently strong direct correlation with a value of R=0.56. It can be said that the system is much simpler, making it easier to monitor and log the various solar radiation parameters.</span>

Targeting the Fusion Process of SARS-CoV-2 Infection by Small Molecule Inhibitors

SARS-CoV-2 is an enveloped virus that requires membrane fusion for entry into host cells. Since the fusion process is relatively conserved among enveloped viruses, we tested our HCV fusion inhibitors, dichlorcyclizine and fluoxazolevir, against SARS-CoV-2.

A Novel Three-Dimensional Computational Method to Assess Rod Contour Deformation and to Map Bony Fusion in a Lumbopelvic Reconstruction After En-Bloc Sacrectomy

Introduction: En-bloc resection of a primary malignant sacral tumor with wide oncological margins impacts the biomechanics of the spinopelvic complex, deteriorating postoperative function. The closed-loop technique (CLT) for spinopelvic fixation (SPF) uses a single U-shaped rod to restore the spinopelvic biomechanical integrity. The CLT method was designed to provide a non-rigid fixation, however this hypothesis has not been previously tested. Here, we establish a computational method to measure the deformation of the implant and characterize the bony fusion process based on the 6-year follow-up (FU) data.Materials and Methods: Post-operative CT scans were collected of a male patient who underwent total sacrectomy at the age of 42 due to a chordoma. CLT was used to reconstruct the spinopelvic junction. We defined the 3D geometry of the implant construct. Using rigid registration algorithms, a common coordinate system was created for the CLT to measure and visualize the deformation of the construct during the FU. In order to demonstrate the cyclical loading of the construct, the patient underwent gait analysis at the 6th year FU. First, a region of interest (ROI) was selected at the proximal level of the construct, then the deformation was determined during the follow-up period. In order to investigate the fusion process, a single axial slice-based voxel finite element (FE) mesh was created. The Hounsfield values (HU) were determined, then using an empirical linear equation, bone mineral density (BMD) values were assigned for every mesh element, out of 10 color-coded categories (1st category = 0 g/cm3, 10th category 1.12 g/cm3).Results: Significant correlation was found between the number of days postoperatively and deformation in the sagittal plane, resulting in a forward bending tendency of the construct. Volume distributions were determined and visualized over time for the different BMD categories and it was found that the total volume of the elements in the highest BMD category in the first postoperative CT was 0.04 cm3, at the 2nd year, FU was 0.98 cm3, and after 6 years, it was 2.30 cm3.Conclusion: The CLT provides a non-rigid fixation. The quantification of implant deformation and bony fusion may help understate the complex lumbopelvic biomechanics after sacrectomy.

Synaptotagmin-1 C2B domains cooperatively stabilize the fusion stalk via a master-servant mechanism

Synaptotagmin-1 is a low-affinity Ca2+ sensor that triggers synchronous vesicle fusion. It contains two similar C2 domains (C2A and C2B) that cooperate in membrane binding, being the C2B domain the main responsible for the membrane fusion process due to its polybasic patch KRLKKKKTTIKK (321-332). In this work, a master-servant mechanism between two identical C2B domains is shown to control the formation of the fusion stalk. Two regions in C2B are essential for the process, the well-known polybasic patch and a recently described pair of arginines (398,399). The master domain shows strong PIP2 interactions with its polybasic patch and its pair of arginines. At the same time, the servant analogously cooperates with the master to reduce the total work to form the fusion stalk. The strategic mutation (T328E,T329E) in both master and servant domains disrupts the cooperative mechanism, drastically increasing the free energy needed to induce the fusion stalk, however with negligible effects on the master domain interactions with PIP2. These data point to a difference in the behavior of the servant domain, which is unable to sustain its PIP2 interactions neither through its polybasic patch nor through its pair of arginines, in the end losing its ability to assist the master in the formation of the fusion stalk.

Theoretical Investigation of the Fusion Process of Mono-Cages to Tri-Cages with CH4/C2H6 Guest Molecules in sI Hydrates

Owing to a stable and porous cage structure, natural gas hydrates can store abundant methane and serve as a potentially natural gas resource. However, the microscopic mechanism of how hydrate crystalline grows has not been fully explored, especially for the structure containing different guest molecules. Hence, we adopt density functional theory (DFT) to investigate the fusion process of structure I hydrates with CH4/C2H6 guest molecules from mono-cages to triple-cages. We find that the volume of guest molecules affects the stabilities of large (51262, L) and small (512, s) cages, which are prone to capture C2H6 and CH4, respectively. Mixed double cages (small cage and large cage) with the mixed guest molecules have the highest stability and fusion energy. The triangular triple cages exhibit superior stability because of the three shared faces, and the triangular mixed triple cages (large-small-large) structure with the mixed guest molecules shows the highest stability and fusion energy in the triple-cage fusion process. These results can provide theoretical insights into the growth mechanism of hydrates with other mono/mixed guest molecules for further development and application of these substances.

MRE11 and UBR5 Co-Operate to Suppress RNF168-Mediated Fusion of Dysfunctional Telomeres

TRF2 is part of the shelterin complex that hides telomeric DNA ends and prevents the activation of the cNHEJ pathway that can lead to chromosomal fusion. TRF2, however, also actively suppresses the cNHEJ pathway by recruiting two proteins, MRE11 and UBR5. MRE11 binds BRCC3, which in turn deubiquitinates γH2AX deposited at exposed telomeric DNA ends and limits RNF168 recruitment to the telomere. UBR5, in contrast directly ubiquitinates and destroys RNF168. The loss of telomeric RNF168 in turn blocks the subsequent recruitment of 53BP1 and prevents the cNHEJ-mediated fusion of chromosomes with exposed telomeric DNA ends. Although MRE11 and UBR5 are both involved in the control of telomeric RNF168 levels and the chromosome fusion process, their relative contributions have not been directly addressed. To do so we genetically suppressed MRE11 and UBR5 alone or in combination in glioma cell lines which we previously showed contained dysfunctional telomeres that were dependent on TRF2 for suppression of telomeric fusion and monitored the effects on events associated with telomere fusion. We here show that while suppression of either MRE11 or UBR5 alone had minimal effects on RNF168 telomeric accumulation, 53BP1 recruitment, and telomeric fusion, their combined suppression led to significant increases in RNF168 and 53BP1 telomeric recruitment and telomeric fusion and eventually cell death, all of which were reversible by suppression of RNF168 itself. These results show that MRE11 and UBR5 co-operate to suppress fusion at dysfunctional telomeres.