Effect of ultrasonication on selected enzymes from Neurospora crassa mycelia

Effect of ultrasonication on selected enzymes from Neurospora crassa myceli

Germination and enzyme activities by the aging of Neurospora conidia in water

Effect of storage in water on germination and enzyme activitie

Migrating to Cloud-Native Architectures Using Microservices: An Experience Report

Migration to the cloud has been a popular topic in industry and academia in recent years. Despite many benefits that the cloud presents, such as high availability and scalability, most of the on-premise application architectures are not ready to fully exploit the benefits of this environment, and adapting them to this environment is a non-trivial task. Microservices have appeared recently as novel architectural styles that are native to the cloud. These cloud-native architectures can facilitate migrating on-premise architectures to fully benefit from the cloud environments because non-functional attributes, like scalability, are inherent in this style. The existing approaches on cloud migration does not mostly consider cloud-native architectures as their first-class citizens. As a result, the final product may not meet its primary drivers for migration. In this paper, we intend to report our experience and lessons learned in an ongoing project on migrating a monolithic on-premise software architecture to microservices. We concluded that microservices is not a one-fit-all solution as it introduces new complexities to the system, and many factors, such as distribution complexities, should be considered before adopting this style. However, if adopted in a context that needs high flexibility in terms of scalability and availability, it can deliver its promised benefits

Suborbital Payload Testing Aboard Level 3 Rocket Research Platform

Embry-Riddle Aeronautical University (ERAU) has launched several suborbital scientific payloads aboard Blue Origin’s New Shepard in 2017 and 2019. Students continue gaining hands-on experience in rocket design and construction, and payload integration and testing of future and more mature payloads to be launched into space. A Level 3 Rocket is being designed and developed at ERAU to serve as a scaled-down model research platform for launching and testing of payloads that will be later flown in commercial suborbital platforms such as Blue Origin’s New Shepard and PLD space Miura 1 rockets. Computer simulations were conducted to calculate the key parameters such as flight trajectory profiles, stability and flight velocities for different rocket motors configurations. A preliminary design of the rocket was developed using Computer-Aided Design (CAD) software. The rocket will accommodate multiple payloads (Cubesats, NanoLabs, TubeSats) designed and developed in the Payload Applied, Technology and Operations (PATO) laboratory. The rocket will be primarily constructed of carbon fiber composite as it has a high strength to weight ratio. These simulations are used to select a suitable motor for the rocket according to the flight requirements and landing restrictions. This prospective Level 3 Rocket is referred to as Suborbital Technology Experimental Vehicle for Exploration (STEVE). Rocket procedures and results from the design, simulation, construction and assembly will be presented

Portal vein thrombosis, mortality and hepatic decompensation in patients with cirrhosis: A meta-analysis

AIM: To determine the clinical impact of portal vein thrombosis in terms of both mortality and hepatic decompensations (variceal hemorrhage, ascites, portosystemic encephalopathy) in adult patients with cirrhosis. METHODS: We identified original articles reported through February 2015 in MEDLINE, Scopus, Science Citation Index, AMED, the Cochrane Library, and relevant examples available in the grey literature. Two independent reviewers screened all citations for inclusion criteria and extracted summary data. Random effects odds ratios were calculated to obtain aggregate estimates of effect size across included studies, with 95%CI. RESULTS: A total of 226 citations were identified and reviewed, and 3 studies with 2436 participants were included in the meta-analysis of summary effect. Patients with portal vein thrombosis had an increased risk of mortality (OR = 1.62, 95%CI: 1.11-2.36, P = 0.01). Portal vein thrombosis was associated with an increased risk of ascites (OR = 2.52, 95%CI: 1.63-3.89, P < 0.001). There was insufficient data available to determine the pooled effect on other markers of decompensation including gastroesophageal variceal bleeding or hepatic encephalopathy. CONCLUSION: Portal vein thrombosis appears to increase mortality and ascites, however, the relatively small number of included studies limits more generalizable conclusions. More trials with a direct comparison group are needed

A Phase-Field Model of Spiral Dendritic Growth

Domains of condensed-phase monolayers of chiral molecules exhibit a variety of interesting nonequilibrium structures when formed via pressurization. To model these domain patterns, we add a complex field describing the tilt degree of freedom to an (anisotropic) complex-phase-field solidification model. The resulting formalism allows for the inclusion of (in general, non-reflection symmetric) interactions between the tilt, the solid-liquid interface, and the bond orientation. Simulations demonstrate the ability of the model to exhibit spiral dendritic growth.Comment: text plus Four postscript figure file

Molecular Epidemiology of O139 Vibrio cholerae: Mutation, Lateral Gene Transfer, and Founder Flush

Vibrio cholerae in O-group 139 was first isolated in 1992 and by 1993 had been found throughout the Indian subcontinent. This epidemic expansion probably resulted from a single source after a lateral gene transfer (LGT) event that changed the serotype of an epidemic V. cholerae O1 El Tor strain to O139. However, some studies found substantial genetic diversity, perhaps caused by multiple origins. To further explore the relatedness of O139 strains, we analyzed nine sequenced loci from 96 isolates from patients at the Infectious Diseases Hospital, Calcutta, from 1992 to 2000. We found 64 novel alleles distributed among 51 sequence types. LGT events produced three times the number of nucleotide changes compared to mutation. In contrast to the traditional concept of epidemic spread of a homogeneous clone, the establishment of variant alleles generated by LGT during the rapid expansion of a clonal bacterial population may be a paradigm in infections and epidemics

Neuronal mTORC1 inhibition promotes longevity without suppressing anabolic growth and reproduction in C. elegans.

mTORC1 (mechanistic target of rapamycin complex 1) is a metabolic sensor that promotes growth when nutrients are abundant. Ubiquitous inhibition of mTORC1 extends lifespan in multiple organisms but also disrupts several anabolic processes resulting in stunted growth, slowed development, reduced fertility, and disrupted metabolism. However, it is unclear if these pleotropic effects of mTORC1 inhibition can be uncoupled from longevity. Here, we utilize the auxin-inducible degradation (AID) system to restrict mTORC1 inhibition to C. elegans neurons. We find that neuron-specific degradation of RAGA-1, an upstream activator of mTORC1, or LET-363, the ortholog of mammalian mTOR, is sufficient to extend lifespan in C. elegans. Unlike raga-1 loss of function genetic mutations or somatic AID of RAGA-1, neuronal AID of RAGA-1 robustly extends lifespan without impairing body size, developmental rate, brood size, or neuronal function. Moreover, while degradation of RAGA-1 in all somatic tissues alters the expression of thousands of genes, demonstrating the widespread effects of mTORC1 inhibition, degradation of RAGA-1 in neurons only results in around 200 differentially expressed genes with a specific enrichment in metabolism and stress response. Notably, our work demonstrates that targeting mTORC1 specifically in the nervous system in C. elegans uncouples longevity from growth and reproductive impairments, and that many canonical effects of low mTORC1 activity are not required to promote healthy aging. These data challenge previously held ideas about the mechanisms of mTORC1 lifespan extension and underscore the potential of promoting longevity by neuron-specific mTORC1 modulation