Introduction: History, biology, physics, cryogens
Richard P. Usatine, Daniel L. Stulberg, Graham B. Colver in Cutaneous Cryosurgery, 2014
The study of cryobiology can be divided into two main areas. Cell preservation covers areas such as the preservation of blood products, gametes, embryos, and organs for transplantation. Cell destruction deals with cold-induced cell and tissue damage, and this underpins the discipline of cryosurgery. Understanding the mechanisms of cell damage is important if maximum benefit is to be gained from treatments. The tissue response to cold injury, which can range from inflammation to total destruction, depends on the severity of freezing. The lesion created by freezing is characterized by coagulation necrosis in the central region with a surrounding, relatively thin, peripheral region in which cell death is apparent. The effects are described as either early, direct or delayed, indirect. Before a detailed description is given it is important to emphasize that the effects of cryosurgery are not uniform across the treated area. In the border, or peripheral, zone the cooling rate is slow, the duration of freezing is short, the final temperature is in the range 0 to −10°C, and warming is rather rapid. In this zone, some cells are necrotic, others are apoptotic, and others may survive. Many cells close to the 0°C isotherm will survive and it is in this range that differences in cell sensitivity to freezing injury become evident. Much of the basic science in this area is “cell” science and not necessarily directly applicable to whole tissues and organs. It will be seen how delayed changes such as hypoxia then influence the damage done by the primary effects of ice formation.
Developing a Toxicology Evaluation Plan for Transdermal Delivery Systems
Francis N. Marzulli, Howard I. Maibach in Dermatotoxicology Methods: The Laboratory Worker’s Vade Mecum, 2019
Many other indicators of cell viability have been used as well. Assays that monitor cell membrane integrity have been widely recognized as indicators of irreversible cell damage. Such assays include nuclear and cellular staining by membrane impermeant dyes (e.g., trypan blue and propidium iodide), release of trapped cytoplasmic probes (fluorescein and derivatives), and leakage of intracellular enzymes, such as lactate dehydrogenase and acid phosphatase (Mosmann et al., 1986; Martin and Clynes, 1991; Nieminen et al., 1992; Eun et al., 1994). Other methods assess the release of inflammation markers such as prostaglandin Eo or interleukin-1 alpha (Dickson et al., 1993). Unfortunately, most of these assays are not readily adaptable to large-scale cytotoxicity screening.
Assessing and responding to sudden deterioration in the adult
Nicola Neale, Joanne Sale in Developing Practical Nursing Skills, 2022
There are four stages of shock: initial, compensatory, progressive and refractory (Summers 2020) (Garretson and Malberti 2007). Initial – the body shows signs of reduced cardiac output.Compensatory – the body attempts to restore homeostasis and improve tissue perfusion.Progressive – the body loses its ability to compensate, bringing about acidosis and electrolyte imbalance.Refractory – irreversible cell damage occurs and the body’s organs are affected.
Pretreatment of bone mesenchymal stem cells with miR181-c facilitates craniofacial defect reconstruction via activating AMPK-Mfn1 signaling pathways
Published in Journal of Receptors and Signal Transduction, 2019
Longkun Fan, Jingxian Wang, Chao Ma
To investigate whether oxidative stress regulated the miR-181c level in BMSC, cells were treated with oxidative stress at different concentrations for 24 h, and the miR-181c level was determined by qRT-PCR. The results illuminated that oxidative injury markedly inhibited the transcription of miR-181c (Figure 1(A))[39]. In accordance with these data, the cell viability of BMSC was also significantly inhibited after treatment with different doses of H2O2 (Figure 1(B)). To understand whether miR-181c downregulation was associated with cell damage, miR-181c mimics were used to incubate with BMSC under H2O2. Then, cell viability was measured via LDH release assay. The results showed that miR-181c mimics obviously attenuated LDH release in BMSC when compared to the H2O2-treated cells (Figure 1(C)). Cell damage may be resulted from cell death. Accordingly, PI staining was used to observe cell death after supplementation with miR-181c in the H2O2-induced oxidative stress environment. In Figure 1(D,E), we could find that H2O2 treatment increased the percentage of PI-positive cells, indicative of increased cell death in the oxidative stress environment. Interestingly, miR-181c treatment significantly reduced the ratio of PI-positive cells, suggesting that miR-181c had an anti-apoptotic effect of BMSC in the oxidative stress environment.
Effects of radiofrequency radiation on apoptotic and antiapoptotic factors in colorectal cancer cells
Published in Electromagnetic Biology and Medicine, 2022
Sanem Gökçen, Berrak Kurt, Yusuf Küçükbağrıaçık, Elcin Ozgur-Buyukatalay, Görkem Kismali
In this study, the effects of intermittent non-thermal exposure to RFR under different exposure conditions (15 min on 15 min off for 1 h, 1 h on 1 h off for 3 h, at 2.5 GHz frequency) on cell viability and apoptosis in colon adenocarcinoma cells were analyzed. Cell damage occurs when the adaptation mechanisms that come into play in the presence of stress in normal cell homeostasis are insufficient. In chronic exposure to stress, irreversible cell damage, and death occur. Cell death can be defined morphologically or biochemically by various markers. There are two main cell death pathways that differ in appearance and functioning in physiological and pathological conditions that are necrosis and apoptosis (Gokhan et al. 2020). Results of the study showed that cell proliferation decreased due to RFR exposure for 3 h while cell viability rates did not change for 1 h RFR exposure with respect to respective sham groups (Figure 1). In addition, early and late apoptosis increased during 1 hour and 3 hours of exposure to 2.5 GHz continuous wave exposure; however, it reveals that 3 GPP modulated 2.5 GHz RFR led to decrease in early apoptosis. Necrotic responses did not change due to modulated signal exposure while continuous wave RFR caused an increase in necrosis.
Anaesthesia for a patient with Friedreich’s ataxia undergoing emergency tibia interlocking nail insertion
Published in Egyptian Journal of Anaesthesia, 2022
Ahmed Abd Elmohsen Bedewy
Friedreich's ataxia is a disorder that affects a gene (FXN) on chromosome 9, which produces an important protein (frataxin). Low frataxin levels lead to insufficient biosynthesis of iron–sulfur clusters that are needed for mitochondrial electron transport and iron metabolism. This leads to cell damage and degeneration. Degeneration occurs in sensory nerves more than motor nerves. Similar degenerative changes occur in cardiac cells and pancreatic cells causing left ventricular hypertrophy and dilatation and diabetes mellitus. Friedreich's ataxia is the most common inherited ataxia with a prevalence of 1 in 30,000–50,000 and a carrier frequency of 1 in 90–110. The classic Friedreich’s ataxia phenotype is due to a homozygous GAA (guanine, adenine, adenine) triplet repeat expansion in intron 1 of the frataxin gene [3–6].
Related Knowledge Centers
- Coagulation
- Glucose
- Necrosis
- Virus
- Hypoxia
- Ischemia
- Apoptosis
- Homeostasis
- Cell
- Adenosine Triphosphate