Rancang Bangun Desain Internet Of Things untuk Pemantauan Kualitas Udara pada Studi Kasus Polusi Udara

Build, design and develop an Internet of Things design to monitor air quality in thewild with air pollution case studies. By utilizing the ESP-8266 type wifi modulemicrocontroller as the control center for the devices built by adding an IC4051 AnalogMultiplexer as a branching process from 1 analog channel to 7 analog channels. There are5 sensors used, namely CO (MQ-7), CO2 (Analog Infrared CO2), Dust Sensors (PM10),DHT-11 (Temperature & Humidity) and Wind speed & direction. Data recording locationand data monitoring using third party protocol, namely Ubidots.The research was conducted in 2 different locations with the time determined, namelyin the area of the UPR Informatics Engineering Department area and also in the village ofTanjung Taruna, Jabiren Raya District, Pulang Pisau Regency along with the Team of theKopernik Bali Foundation.The results of the study will be analyzed using the AQI (Air Quality Index) standardwhich is also the same as that of the BMKG as an air quality index index. By using realtimeinternet of things technology, it can make it easy to get information about the level of airquality in the wild quickly, efficiently, and the monitoring process can be done anywhereand anytime

RANCANG BANGUN DESAIN INTERNET OF THINGS UNTUK PEMANTAUAN KUALITAS UDARA PADA STUDI KASUS POLUSI UDARA

Build, design and develop an Internet of Things design to monitor air quality in thewild with air pollution case studies. By utilizing the ESP-8266 type wifi modulemicrocontroller as the control center for the devices built by adding an IC4051 AnalogMultiplexer as a branching process from 1 analog channel to 7 analog channels. There are5 sensors used, namely CO (MQ-7), CO2 (Analog Infrared CO2), Dust Sensors (PM10),DHT-11 (Temperature & Humidity) and Wind speed & direction. Data recording locationand data monitoring using third party protocol, namely Ubidots.The research was conducted in 2 different locations with the time determined, namelyin the area of the UPR Informatics Engineering Department area and also in the village ofTanjung Taruna, Jabiren Raya District, Pulang Pisau Regency along with the Team of theKopernik Bali Foundation.The results of the study will be analyzed using the AQI (Air Quality Index) standardwhich is also the same as that of the BMKG as an air quality index index. By using realtimeinternet of things technology, it can make it easy to get information about the level of airquality in the wild quickly, efficiently, and the monitoring process can be done anywhereand anytime

The economic trade-offs of large language models: A case study

Contacting customer service via chat is a common practice. Because employing customer service agents is expensive, many companies are turning to NLP that assists human agents by auto-generating responses that can be used directly or with modifications. Large Language Models (LLMs) are a natural fit for this use case; however, their efficacy must be balanced with the cost of training and serving them. This paper assesses the practical cost and impact of LLMs for the enterprise as a function of the usefulness of the responses that they generate. We present a cost framework for evaluating an NLP model's utility for this use case and apply it to a single brand as a case study in the context of an existing agent assistance product. We compare three strategies for specializing an LLM - prompt engineering, fine-tuning, and knowledge distillation - using feedback from the brand's customer service agents. We find that the usability of a model's responses can make up for a large difference in inference cost for our case study brand, and we extrapolate our findings to the broader enterprise space.Comment: Paper to be published at the Association for Computational Linguistics in the Industry Track 202

Chemical compound 31002 stimulates cardiomyogenic differentiation of embryonic stem cells

Embryonic stem cells (ESCs) are an emerging source for cell-based therapies aimed at repairing damaged organ tissues; however, the efficiency of directed differentiation is low and refinement of differentiation protocols is hampered by incomplete understanding of the mechanisms involved in this process. To find new compounds which can improve the efficiency of directed differentiation of ESCs to cardiomyocytes, we screened several thousand chemical compounds and identified a promising group. All of the compounds found have a common structure of 1H-pyrrole,2,2'-(phenylmethylene)bis. Here we report the potential mechanism of action for 31002 which showed the strongest activity among the compounds selected. In the presence of 31002, 15 times more cardiomyocytes differentiated from ESCs, i.e., 3.5% to 52% of total differentiated cells. Moreover, the cardiomyocytes showed functional characteristics including rhythmic beating and marker gene expression. 31002 inhibited the down-regulation of genes related to the three germ layers in the late stage of ESCs differentiation, implying that 31002 supports a continuous fate commitment of undifferentiated ESCs to the cardiac lineage by prolonging the three germ layer stages. Therefore, compounds in this group, including 31002, might be useful as directed cardiomyogenic differentiation-inducers to produce cells for use in cell therapy aimed at restoring damaged heart tissue

Numerous proteins with unique characteristics are degraded by the 26S proteasome following monoubiquitination

The "canonical" proteasomal degradation signal is a substrateanchored polyubiquitin chain. However, a handful of proteins were shown to be targeted following monoubiquitination. In this study, we established-in both human and yeast cells-a systematic approach for the identification of monoubiquitination-dependent proteasomal substrates. The cellular wild-type polymerizable ubiquitin was replaced with ubiquitin that cannot form chains. Using proteomic analysis, we screened for substrates that are nevertheless degraded under these conditions compared with those that are stabilized, and therefore require polyubiquitination for their degradation. For randomly sampled representative substrates, we confirmed that their cellular stability is in agreement with our screening prediction. Importantly, the two groups display unique features: monoubiquitinated substrates are smaller than the polyubiquitinated ones, are enriched in specific pathways, and, in humans, are structurally less disordered. We suggest that monoubiquitination-dependent degradation is more widespread than assumed previously, and plays key roles in various cellular processes

Numerous proteins with unique characteristics are degraded by the 26S proteasome following monoubiquitination

The "canonical" proteasomal degradation signal is a substrate-anchored polyubiquitin chain. However, a handful of proteins were shown to be targeted following monoubiquitination. In this study, we established-in both human and yeast cells-a systematic approach for the identification of monoubiquitination-dependent proteasomal substrates. The cellular wild-type polymerizable ubiquitin was replaced with ubiquitin that cannot form chains. Using proteomic analysis, we screened for substrates that are nevertheless degraded under these conditions compared with those that are stabilized, and therefore require polyubiquitination for their degradation. For randomly sampled representative substrates, we confirmed that their cellular stability is in agreement with our screening prediction. Importantly, the two groups display unique features: monoubiquitinated substrates are smaller than the polyubiquitinated ones, are enriched in specific pathways, and, in humans, are structurally less disordered. We suggest that monoubiquitination-dependent degradation is more widespread than assumed previously, and plays key roles in various cellular processes

Induced pluripotent stem cell-derived cardiomyocytes in studies of inherited arrhythmias

The discovery of the genetic basis of inherited arrhythmias has paved the way for an improved understanding of arrhythmogenesis in a wide spectrum of life-threatening conditions. In vitro expression of mutations and transgenic animal models have been instrumental in enhancing this understanding, but the applicability of results to the human heart remains unknown. The ability to differentiate induced pluripotent stem cells (iPSs) into cardiomyocytes enables the potential to generate patient-specific myocytes, which could be used to recapitulate the features of inherited arrhythmias in the context of the patient's genetic background. Few studies have been reported on iPS-derived myocytes obtained from patients with heritable arrhythmias, but they have demonstrated the applicability of this innovative approach to the study of inherited arrhythmias. Here we review the results achieved by iPS investigations in arrhythmogenic syndromes and discuss the existing challenges to be addressed before the use of iPS-derived myocytes can become a part of personalized management of inherited arrhythmia

Inhibition of AP-1 signaling by JDP2 overexpression protects cardiomyocytes against hypertrophy and apoptosis induction

AimsExpression and activity of the transcription factor AP-1 are enhanced during cardiac remodelling and heart failure progression. In order to test if AP-1 inhibition may limit processes contributing to cardiac remodelling, ventricular cardiomyocytes of mice with cardiac overexpression of the AP-1 inhibitor JDP2 were analysed under stimulation of hypertrophy, apoptosis, or contractile function.Methods and resultsThree models of JDP2 overexpressing mice were analysed: JDP2 was overexpressed either life-long, for 7 weeks, or 1 week. Then cardiomyocytes were isolated and stimulated with β-adrenoceptor agonist isoprenaline (ISO, 50 nM). This enhanced cross-sectional area and the rate of protein synthesis in WT but not in JDP2 overexpressing cardiomyocytes. To induce apoptosis, cardiomyocytes were stimulated with 3 ng/mL TGFβ1. Again, JDP2 overexpression prevented apoptosis induction compared with WT cells. Determination of contractile function under electrical stimulation at 2 Hz revealed enhancement of cell shortening, and contraction and relaxation velocities under increasing ISO concentrations (0.3-30 nM) in WT cells. This inotropic effect was abrogated in JDP2 overexpression cells. Responsiveness to increased extracellular calcium concentrations was also impaired in JDP2 overexpressing cardiomyocytes. Simultaneously, a reduction of SERCA expression was found in JDP2 mice.ConclusionA central role of AP-1 in the induction of hypertrophy and apoptosis in cardiomyocytes is demonstrated. Besides these protective effects of AP-1 inhibition on factors of cardiac remodelling, AP-1-inhibition impairs contractile function. Therefore, AP-1 acts as a double-edged sword that mediates mal-adaptive cardiac remodelling, but is required for maintaining a proper contractile function of cardiomyocytes. © 2013 Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2013