Dynamic Analysis of Drug-Induced Cytotoxicity Using Chip-Based Dielectrophoretic Cell Immobilization Technology

2011 ◽  
Vol 83 (6) ◽  
pp. 2133-2144 ◽  
Author(s):  
Khashayar Khoshmanesh ◽  
Jin Akagi ◽  
Saeid Nahavandi ◽  
Joanna Skommer ◽  
Sara Baratchi ◽  
...  
Author(s):  
Hao Gao ◽  
Jiasheng Lu ◽  
Yujia Jiang ◽  
Yan Fang ◽  
Yunhan Tang ◽  
...  

2016 ◽  
Vol 219 ◽  
pp. 725-737 ◽  
Author(s):  
Gopalakrishnan Kumar ◽  
Ackmez Mudhoo ◽  
Periyasamy Sivagurunathan ◽  
Dillirani Nagarajan ◽  
Anish Ghimire ◽  
...  

2019 ◽  
Vol 25 (6) ◽  
pp. 807-818 ◽  
Author(s):  
Pattaraporn Kunapongkiti ◽  
Chaiwat Rongsayamanont ◽  
Panida Nayramitsattha ◽  
Tawan Limpiyakorn

Nitritation, the oxidation of ammonia to nitrite without subsequent oxidation to nitrate, is a starting step for nitrite-based nitrogen removal approaches. This process can be induced by maintaining specific operating conditions that facilitate ammonia oxidation but deteriorate nitrite oxidation. In recent years, a number of publications have demonstrated the ability of cell immobilization to maintain nitritation and an oxygen-limiting strategy was suggested to be a key to the success of the approach. However, several aspects related to the success and failure of such systems remains unclear and requires further in-depth clarification. This review provides current information on the utilization of cell immobilization in nitritation reactors. Common operating strategies that promote nitritation by controlling environmental conditions are summarized in the first part of the review. The application of cell immobilization, including cell attachment, cell granulation, and cell entrapment systems, as well as microenvironments, and microbial distributions within cell immobilization matrices, are elaborated in the middle part of the review. Problems encountered in the operation of nitritation reactors using cell immobilization are discussed as opportunities for further research at the end of the review.


2020 ◽  
Vol 59 (39) ◽  
pp. 17026-17034 ◽  
Author(s):  
Jiasheng Lu ◽  
Wenfang Peng ◽  
Yang Lv ◽  
Yujia Jiang ◽  
Bin Xu ◽  
...  

Author(s):  
F. G. Zaki ◽  
E. Detzi ◽  
C. H. Keysser

This study represents the first in a series of investigations carried out to elucidate the mechanism(s) of early hepatocellular damage induced by drugs and other related compounds. During screening tests of CNS-active compounds in rats, it has been found that daily oral administration of one of these compounds at a dose level of 40 mg. per kg. of body weight induced diffuse massive hepatic necrosis within 7 weeks in Charles River Sprague Dawley rats of both sexes. Partial hepatectomy enhanced the development of this peculiar type of necrosis (3 weeks instead of 7) while treatment with phenobarbital prior to the administration of the drug delayed the appearance of necrosis but did not reduce its severity.Electron microscopic studies revealed that early development of this liver injury (2 days after the administration of the drug) appeared in the form of small dark osmiophilic vesicles located around the bile canaliculi of all hepatocytes (Fig. 1). These structures differed from the regular microbodies or the pericanalicular multivesicular bodies. They first appeared regularly rounded with electron dense matrix bound with a single membrane. After one week on the drug, these vesicles appeared vacuolated and resembled autophagosomes which soon developed whorls of concentric lamellae or cisterns characteristic of lysosomes (Fig. 2). These lysosomes were found, later on, scattered all over the hepatocytes.


Author(s):  
R. H. Liss

Piperacillip (PIP) is b-[D(-)-α-(4-ethy1-2,3-dioxo-l-piperzinylcar-bonylamino)-α-phenylacetamido]-penicillanate. The broad spectrum semisynthetic β-lactam antibiotic is believed to effect bactericidal activity through its affinity for penicillin-binding proteins (PBPs), enzymes on the bacterial cytoplasmic membrane that control elongation and septation during cell growth and division. The purpose of this study was to correlate penetration and binding of 14C-PIP in bacterial cells with drug-induced lethal changes assessed by microscopic, microbiologic and biochemical methods.The bacteria used were clinical isolates of Escherichia coli and Pseudomonas aeruginosa (Figure 1). Sensitivity to the drug was determined by serial tube dilution in Trypticase Soy Broth (BBL) at an inoculum of 104 organisms/ml; the minimum inhibitory concentration of piperacillin for both bacteria was 1 μg/ml. To assess drug binding to PBPs, the bacteria were incubated with 14C-PIP (5 μg/0.09 μCi/ml); controls, in drug-free medium.


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