scholarly journals Polymer-Based Functional Cantilevers Integrated with Interdigitated Electrode Arrays—A Novel Platform for Cardiac Sensing

Micromachines ◽  
2020 ◽  
Vol 11 (4) ◽  
pp. 450 ◽  
Author(s):  
Pooja P. Kanade ◽  
Nomin-Erdene Oyunbaatar ◽  
Dong-Weon Lee
Keyword(s):  
Cardiac Toxicity ◽  
Toxicity Tests ◽  
Dual Function ◽  
Electrode Arrays ◽  
Contraction Force ◽  
Drug Induced ◽  
Cantilever Deflection ◽  
Biomedical Device ◽  
Photosensitive Polymer ◽  
Common Causes

Heart related ailments are some of the most common causes for death in the world, and some of the causes are cardiac toxicity due to drugs. Several platforms have been developed in this regard over the years that can measure electrical or mechanical behavior of cardiomyocytes. In this study, we have demonstrated a biomedical device that can simultaneously measure electrophysiology and contraction force of cardiomyocytes. This dual-function device is composed of a photosensitive polymer-based cantilever, with a pair of metal-based interdigitated electrodes on its surface, such that the cantilever can measure the contraction force of cardiomyocytes and the electrodes can measure the impedance between cells and substrate. The cantilever is patterned with microgrooves so that the cardiomyocytes can align to the cantilever in order to make a higher cantilever deflection in response to contraction force. Preliminary experimental results have identified the potential for use in the drug-induced cardiac toxicity tests, and further optimization is desirable to extend the technique to various bio-sensor areas.

Enhancement of Cardiac Contractility Using Gold-coated SU-8 Cantilevers and Their Application to Drug-induced Cardiac Toxicity Tests

The Analyst ◽  
2021 ◽  
Author(s):  
Jong Yun Kim ◽  
Arunkumar Shanmugasundaram ◽  
Dong-Weon Lee
Keyword(s):  
Cardiac Toxicity ◽  
Cardiac Contractility ◽  
Toxicity Tests ◽  
Drug Induced

Herein, we propose an array of gold (Au)-coated SU-8 cantilevers with microgrooves for improved maturation of cardiomyocytes and describe its applications to drug-induced cardiac toxicity tests. Firstly, we evaluated the...

scholarly journals Analysis of common causes of liver damage among children 12 years and younger in Weifang

2021 ◽  
Vol 49 (4) ◽  
pp. 030006052110066
Author(s):  
Qinghong Meng ◽  
Na Li ◽  
Lianmei Yuan ◽  
Xiaona Gao
Keyword(s):  
Liver Damage ◽  
Epstein Barr Virus ◽  
Metabolic Diseases ◽  
Unknown Etiology ◽  
Severe Liver ◽  
Drug Induced ◽  
Barr Virus ◽  
Common Causes ◽  
Severe Liver Damage ◽  
Epstein Barr

Aims To explore the causes of liver damage among children 12 years and younger in Weifang and to provide a theoretical basis for early diagnosis of liver damage in children. Methods Retrospective study of clinical data from pediatric patients (age ≤12 years) with liver damage in diagnosed at Weifang People's Hospital from June 2010 to May 2020. Results A total of 2632 children (1572 boys, 1060 girls) aged ≤12 years were diagnosed with liver damage including infectious liver damage (2100 cases), non-infectious liver damage (446 cases) and liver damage of unknown etiology (86 cases). The most common causes of infectious liver damage were viral infection (1515 cases), Mycoplasma pneumoniae infection (343 cases), and bacterial infection (197 cases). The most common causes of viral liver damage were Epstein–Barr virus, cytomegalovirus, and enterovirus. The most common causes of non-infectious liver damage were drug-induced liver damage, Kawasaki disease, and genetic metabolic diseases. There were 31 cases of severe liver damage. Conclusion There were many causes of liver damage among children in Weifang. Infections, and especially viral infections such as Epstein–Barr virus, were the most common causes of liver damage. Severe liver damage was primarily caused by drugs or poisons.

scholarly journals Chemopreventive role of Coriandrum sativum against gentamicin-induced renal histopathological damage in rats

2015 ◽  
Vol 8 (2) ◽  
pp. 99-102 ◽  
Author(s):  
Abhijeet Lakhera ◽  
Aditya Ganeshpurkar ◽  
Divya Bansal ◽  
Nazneen Dubey
Keyword(s):  
Acute Toxicity ◽  
Natural Antioxidants ◽  
Positive Control ◽  
Coriandrum Sativum ◽  
Drug Induced ◽  
Common Causes ◽  
Histopathological Studies ◽  
Oecd Guideline ◽  
Important Medicinal Plant

Abstract Drug induced nephrotoxicity is one of the most common causes of renal failure. Gentamicin belongs to aminoglycosides, which elicit nephrotoxic potential. Natural antioxidants from plants demonstrate a number of biotherapeutic activities. Coriander is an important medicinal plant known for its hepatoprotective, diuretic, carminative, digestive and antihelminthic potential. This study was designed to investigate whether the extract of Coriandrum sativum ameliorates the nephrotoxicity induced by gentamicin in rats. Dried coriander powder was coarsely grinded and subjected to defatting by petroleum ether and further with ethyl acetate. The extract was filtered and subjected to phytochemical and phytoanalytical studies. Acute toxicity in Wistar rats was determined by the OECD Guideline (423). Animals were divided into four groups. The first group served as positive control, while the second group was toxic control (gentamicin treated). The third and fourth group were treated with the extract (200 and 400 mg/kg gentamicin). After 8 days, the animals were sacrificed and biochemical and histopathological studies were carried out. Phytochemical screening of the extract demonstrated Coriandrum sativum to be rich in flavonoids, polyphenolics and alkaloids. Results of acute toxicity suggested the use of 200 mg/kg and 400 mg/kg for Coriandrum sativum in the study. Coriandrum sativum extract at the dose of 400 mg/kg significantly (p<0.01) decreased creatinine levels in the animals, along with a decrease in serum urea and blood urea nitrogen. Treatment with Coriandrum sativum extract ameliorated renal histological lesions. It is concluded that Coriandrum sativum is a potential source of nephroprotective phytochemical activity, with flavonoids and polyphenols as the major components.

Drug-induced cardiac toxicity: emphasizing the role of electrocardiography in clinical research and drug development

2004 ◽  
Vol 37 (1) ◽  
pp. 19-24 ◽  
Author(s):  
Ihor Gussak ◽  
Jeffrey Litwin ◽  
Robert Kleiman ◽  
Scott Grisanti ◽  
Joel Morganroth
Keyword(s):  
Drug Development ◽  
Clinical Research ◽  
Cardiac Toxicity ◽  
Drug Induced

scholarly journals Intermittent Starvation Extends the Functional Lifetime of Primary Human Hepatocyte Cultures

2020 ◽  
Vol 174 (2) ◽  
pp. 266-277
Author(s):  
Matthew D Davidson ◽  
Salman R Khetani
Keyword(s):  
Drug Exposure ◽  
Adenosine Monophosphate ◽  
Human Hepatocyte ◽  
Toxicity Tests ◽  
Drug Induced ◽  
Nonparenchymal Cells ◽  
Primary Human Hepatocyte ◽  
Serum Hormone

Abstract Primary human hepatocyte (PHH) cultures have become indispensable to mitigate the risk of adverse drug reactions in human patients. In contrast to dedifferentiating monocultures, coculture with nonparenchymal cells maintains PHH functions for 2–4 weeks. However, because the functional lifespan of PHHs in vivo is 200–400 days, it is desirable to further prolong PHH functions in vitro toward modeling chronic drug exposure and disease progression. Fasting has benefits on the longevity of organisms and the health of tissues such as the liver. We hypothesized that a culturing protocol that mimics dynamic fasting/starvation could activate starvation pathways and prolong PHH functional lifetime. To mimic starvation, serum and hormones were intermittently removed from the culture medium of micropatterned cocultures (MPCCs) containing PHHs organized onto collagen domains and surrounded by 3T3-J2 murine fibroblasts. A weekly 2-day starvation optimally prolonged PHH functional lifetime for 6+ weeks in MPCCs versus a decline after 3 weeks in nonstarved controls. The 2-day starvation also enhanced the functions of PHH monocultures for 2 weeks, suggesting direct effects on PHHs. In MPCCs, starvation activated 5' adenosine monophosphate-activated protein kinase (AMPK) and restricted fibroblast overgrowth onto PHH islands, thereby maintaining hepatic polarity. The effects of starvation on MPCCs were partially recapitulated by activating AMPK using metformin or growth arresting fibroblasts via mitomycin-C. Lastly, starved MPCCs demonstrated lower false positives for drug toxicity tests and higher drug-induced cytochrome-P450 activities versus nonstarved controls even after 5 weeks. In conclusion, intermittent serum/hormone starvation extends PHH functional lifetime toward enabling clinically relevant drug screening.

scholarly journals Subacute cutaneous lupus erythematosus with a possible paraneoplastic association with melanoma

2019 ◽  
Vol 12 (11) ◽  
pp. e230558 ◽  
Author(s):  
Jesse Hirner
Keyword(s):  
Proton Pump Inhibitor ◽  
Lupus Erythematosus ◽  
Cutaneous Lupus Erythematosus ◽  
Laboratory Evaluation ◽  
Topical Steroids ◽  
Subacute Cutaneous Lupus Erythematosus ◽  
Drug Induced ◽  
Dermatology Clinic ◽  
Common Causes ◽  
Cutaneous Lupus

A 52-year-old man was referred to our dermatology clinic for a diagnosis of melanoma. At the time, his melanoma was excised he developed an annular, polycyclic, scaling eruption consistent with subacute cutaneous lupus erythematosus (SCLE). Skin biopsy and laboratory evaluation confirmed this diagnosis. The patient had been using pantoprazole for gastro-oesophageal reflux disease for the last 3 years. The patient’s melanoma was treated surgically, and his SCLE was treated with topical steroids and hydroxychloroquine. His SCLE cleared rapidly, his steroids and hydroxychloroquine were stopped and he remains free of SCLE off of treatment. The parallel course of the patient’s SCLE and melanoma prompted consideration of SCLE as paraneoplastic to melanoma in this case. The clinical picture was complicated by the patient’s use of a proton pump inhibitor, which are common causes of drug-induced SCLE. To our knowledge, this is the first reported case of possible paraneoplastic SCLE associated with melanoma.

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