scholarly journals Real-time environmental monitoring of contaminants using living electronic sensors

2021 ◽  
Author(s):  
Joshua T Atkinson ◽  
Lin Su ◽  
Xu Zhang ◽  
George N. Bennett ◽  
Jonathan Silberg ◽  
...  

Real-time chemical sensing is needed to counter the global threats posed by pollution. We combine synthetic biology and materials engineering to develop a living bioelectronic sensor platform with minute detection times. Escherichia coli was programmed to reduce an electrode in a chemical-dependent manner using a modular, eight-component, synthetic electron transport chain. This strain produced significantly more current upon exposure to thiosulfate, an anion that causes microbial blooms. Incorporating a protein switch into the synthetic pathway and encapsulation of microbes with electrodes and conductive nanomaterials yielded a living bioelectronic sensor that could detect an endocrine disruptor within two minutes in riverine water, implicating the signal as mass transfer limited. These findings provide a new platform for miniature, low-power sensors that safeguard ecological and human health.

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Pengfei Liu ◽  
Jing Yuan ◽  
Yetong Feng ◽  
Xin Chen ◽  
Guangsuo Wang ◽  
...  

AbstractFerroptosis is a novel type of programmed cell death, which is different from apoptosis and autophagic cell death. Recently, ferroptosis has been indicated to contribute to the in vitro neurotoxicity induced by isoflurane, which is one of the most common anesthetics in clinic. However, the in vivo position of ferroptosis in isoflurane-induced neurotoxicity as well as learning and memory impairment remains unclear. In this study, we mainly explored the relationship between ferroptosis and isoflurane-induced learning and memory, as well as the therapeutic methods in mouse model. Our results indicated that isoflurane induced the ferroptosis in a dose-dependent and time-dependent manner in hippocampus, the organ related with learning and memory ability. In addition, the activity of cytochrome c oxidase/Complex IV in mitochondrial electron transport chain (ETC) was increased by isoflurane, which might further contributed to cysteine deprivation-induced ferroptosis caused by isoflurane exposure. More importantly, isoflurane-induced ferroptosis could be rescued by both ferroptosis inhibitor (ferrostatin-1) and mitochondria activator (dimethyl fumarate), which also showed effective therapeutic action against isoflurane-induced learning and memory impairment. Taken together, our data indicate the close association among ferroptosis, mitochondria and isoflurane, and provide a novel insight into the therapy mode against isoflurane-induced learning and memory impairment.


2021 ◽  
Vol 6 (2) ◽  
Author(s):  
Dipti Chavan ◽  
Aniket Kamble ◽  
Aditya Khadsare ◽  
Vaibhav Chougule ◽  
Vaibhav Chougule

Electronics and communication is the most important field. In this paper, we can describe how much safety is in the Automobile industry. In this paper, we are using uno-Arduino. The different types of sensors facilities are also provided using key points. The different sensors are provided to check visitor count. In this system, we can monitor and control all the safety precautions their one IoT web platform. This helps in the proper utilization of drivers and helps in avoiding accidents. This paper can be implemented in any two-wheelers, heavily loaded trucks, small SUVs, compact cars. In our paper, the electronics machine/components will be automatically working with using of Arduino program. The proposed wireless sensor platform is an attempt to develop more safety devices that can be used in multiple areas such as homes, schools, and public utilities to reduce accidents. This Advanced Driver Assists system will provide real-time accident detections and monitoring usage information that helps in real-time by using GSM, GPS, and sensors.


Biologia ◽  
2015 ◽  
Vol 70 (10) ◽  
Author(s):  
Yu Zhang ◽  
Pu Feng ◽  
Jianhong Yang

AbstractIncreased risk of osteoporosis in patients with diabetes mellitus may be related to hyperglycemia. However, the potential mechanisms accounting for diabetic bone disorder remain unresolved. The present study investigated the effects of high glucose-associated osmolality on differentiation of primary rat calvarial osteoblasts. Osteoblastogenic differentiation was determined by bone nodule staining for mineralization assay, enzyme-linked immunosorbent assay for type I collagen production and real-time polymerase chain reaction (PCR) for osteoblastogenic marker gene expression. Adipocytogenic differentiation was assessed by oil red O staining for lipid accumulation and real-time PCR for adipocytogenic marker gene expression. The phosphorylations of protein kinase A (PKA) and Akt were measured with or without specific inhibitors to confirm osmolality involved signalling pathways. The results showed that high glucose-associated osmolality significantly promoted adipocytogenic differentiation, manifested by increased lipid droplet formation and gene expression of adipocytogenic markers including adipocyte fatty acid binding protein (aP2), adipsin and peroxisome proliferator-activated receptor gamma (PPARγ). Meanwhile, high glucose-associated osmolality inhibited osteoblastogenic differentiation, characterized by decreased collagen I protein production and cell mineralization, as well as gene expression of osteoblastogenic markers including collagen I, osteocalcin and runt-related transcription factor 2 (Runx2). More importantly, we demonstrated for the first time that high glucose-associated osmolality induced adipocytogenic differentiation and suppressed osteoblastogenic differentiation in a PKA and phosphatidylinositol 3-kinase (PI3K)/Akt-dependent manner. These results indicated that osmolality was involved in high glucose-induced osteoblast trans-differentiation into adipocyte-like cell and suppression of cellular osmolality could provide novel therapeutic approach for diabetic osteopenia.


2021 ◽  
Vol MA2021-01 (55) ◽  
pp. 1415-1415
Author(s):  
Rocio Arreguin Arreguin Campos ◽  
Kasper Eersels ◽  
Hanne Diliën ◽  
Bart van Grinsven ◽  
Thomas J. Cleij

2020 ◽  
Vol 48 (02) ◽  
pp. 341-356
Author(s):  
Chiu-Mei Lin ◽  
Wei-Jen Fang ◽  
Bao-Wei Wang ◽  
Chun-Ming Pan ◽  
Su-Kiat Chua ◽  
...  

MicroRNA 145 (miR-145) is a critical modulator of cardiovascular diseases. The downregulation of myocardial miR-145 is followed by an increase in disabled-2 (Dab2) expression in cardiomyocytes. (-)-epigallocatechin gallate (EGCG) is a flavonoid that has been evaluated extensively due to its diverse pharmacological properties including anti-inflammatory effects. The aim of this study was to investigate the cardioprotective effects of EGCG under hypoxia-induced stress in vitro and in vivo. The hypoxic insult led to the suppression of miR-145 expression in cultured rat cardiomyocytes in a concentration-dependent manner. Western blotting and real-time PCR were performed. In rat myocardial infarction study, in situ hybridization, and immunofluorescent analyses were adopted. The western blot and real-time PCR data revealed that hypoxic stress with 2.5% O2 suppressed the expression of miR-145 and Wnt3a/[Formula: see text]-catenin in cultured rat cardiomyocytes but augmented Dab2. Treatment with EGCG attenuated Dab2 expression, but increased Wnt3a and [Formula: see text]-catenin in hypoxic cultured cardiomyocytes. Following in vivo myocardial infarction (MI) study, the data revealed the myocardial infarct area reduced by 48.5%, 44.6%, and 48.5% in EGCG (50[Formula: see text]mg/kg) or miR-145 dominant or Dab2 siRNA groups after myocardial infarction for 28 days, respectively. This study demonstrated that EGCG increased miR-145, Wnt3a, and [Formula: see text]-catenin expression but attenuated Dab2 expression. Moreover, EGCG ameliorated myocardial ischemia in vivo. The novel suppressive effect was mediated through the miR-145 and Dab2/Wnt3a/[Formula: see text]-catenin pathways.


2020 ◽  
Vol 26 (8) ◽  
pp. 601-614
Author(s):  
Pooja Sharma ◽  
Hsin-Han Tseng ◽  
Jo-Yu Lynn Lee ◽  
Eing-Mei Tsai ◽  
Jau-Ling Suen

Abstract Endometriosis is an estrogen-dependent chronic inflammatory disease and is associated etiologically with environmental endocrine disruptor (EED) exposure. 4-nonylphenol (NP), a widely found EED, has weak estrogenic activity and modulates plasmacytoid dendritic cell (pDC) function in vitro and in vivo. We aimed to elucidate the immunomodulatory effect of NP on the development of endometriosis, particularly focusing on pDCs. This study established a surgically induced endometriosis murine model (C57BL/6) under conditions of NP treatment that are relevant to the level and route of human exposure. Multi-parametric flow cytometry was used for analysis of infiltrated immune cell subsets in lesions. The results showed that NP exposure significantly promoted endometriotic lesion growth, survival and angiogenesis development of lesions as well as pDC accumulation in the lesions in mice. Adoptive transfer of NP-conditioned pDCs into mice significantly enhanced lesion development and local pDC infiltration, whereas NP-conditioned conventional dendritic cells did not affect lesion growth. In vitro functional analysis showed that NP-conditioned pDCs in lesions expressed high levels of CD36, a scavenger receptor and NP-conditioned splenic pDCs secreted an enhanced level of IL-10 in response to apoptotic cell recognition in a CD36-dependent manner. Furthermore, we observed that local treatment with blocking antibodies against IL-10 and CD36 on the day of surgery significantly inhibited lesion development. NP exposure also altered the estrous cycle in mice. The results suggest that chronic and low-dose exposure to NP enhances endometriotic lesion growth by altering pDC homeostasis and function. This study has important implications for understanding the environment-innate immunity interaction in human endometriosis.


2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Jun-Sub Kim ◽  
Kyuho Jeong ◽  
James M. Murphy ◽  
Yelitza A. R. Rodriguez ◽  
Ssang-Taek Steve Lim

Chemiluminescence (CL) is one of the most useful methods for detecting reactive oxygen species (ROS). Although fluorescence dyes or genetically encoded biosensors have been developed, CL is still used due to its high sensitivity, ease of use, and low cost. While initially established and used to measure high levels of ROS in phagocytic cells, CL assays are not ideal for measuring low levels of ROS. Here, we developed a newly modified CL assay using a chemiluminescent imaging system for measuring low concentrations of ROS in nonphagocytic cells. We found that dissolving luminol in NaOH, rather than DMSO, increased the H2O2-induced CL signal and that the addition of 4-iodophenylboronic acid (4IPBA) further increased CL intensity. Our new system also increased the rate and intensity of the CL signal in phorbol 12-myristate 13-acetate- (PMA-) treated HT-29 colon cancer cells compared to those in luminol only. We were able to quantify ROS levels from both cells and media in parallel using an H2O2standard. A significant benefit to our system is that we can easily measure stimulus-induced ROS formation in a real-time manner and also investigate intracellular signaling pathways from a single sample simultaneously. We found that PMA induced tyrosine phosphorylation of protein tyrosine kinases (PTKs), such as focal adhesion kinase (FAK), protein tyrosine kinase 2 (Pyk2), and Src, and increased actin stress fiber formation in a ROS-dependent manner. Interestingly, treatment with either N-acetyl-L-cysteine (NAC) or diphenyleneiodonium (DPI) reduced the PMA-stimulated phosphorylation of these PTKs, implicating a potential role in cellular ROS signaling. Thus, our newly optimized CL assay using 4IPBA and a chemiluminescent imaging method provides a simple, real-time, and low-cost method for the quantification of low levels of ROS.


2013 ◽  
Vol 19 (2) ◽  
pp. 223-231 ◽  
Author(s):  
Alisa Knapman ◽  
Fe Abogadie ◽  
Peter McIntrye ◽  
Mark Connor

Inhibition of adenylyl cyclase (AC) activity is frequently used to measure µ-opioid receptor (MOR) activation. We sought to develop a simple, rapid assay of AC activity in whole cells that could be used to study MOR signaling. Chinese hamster ovary cells expressing human MOR (CHO-MOR cells) were grown in 96-well plates and loaded with membrane potential–sensitive fluorescent dye. CHO-MOR cells were treated with the AC activator forskolin (FSK), with or without simultaneous application of MOR agonists, and the resulting change in fluorescence was measured. CHO-MOR cells hyperpolarized in response to application of FSK ( pEC50, 7.3) or calcitonin ( pEC50, 9.4). A submaximally effective concentration of FSK (300 nM) caused a 52% ± 2% decrease in fluorescence. Simultaneous application of the opioids DAMGO ( pEC50, 7.4; Emax, 56%), morphine ( pEC50, 7.0; Emax, 61%); and buprenorphine ( pEC50, 8.6; Emax, 24%) inhibited the FSK response in a dose-dependent manner while having no effect by themselves. The effects of DAMGO were blocked by pertussis toxin. This assay represents a simple, robust method for real-time observation of AC inhibition by MOR in CHO cells. It represents an appealing alternative to end-point assays that rely on cAMP accumulation and can avoid potential confounds associated with rapid desensitization of MOR signaling.


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