Although the phenomenon of mitotic catastrophe was first described more than 80 years ago, only recently has this term been used to explain a mechanism of cell death linked to delayed mitosis. Several mechanisms have been suggested for mitotic catastrophe development and cell fate. Depending on molecular perturbations, mitotic catastrophe can end in three types of cell death, namely apoptosis, necrosis, or autophagy. Moreover, mitotic catastrophe can be associated with different types of cell aging, the development of which negatively affects tumor elimination and, consequently, reduces the therapeutic effect. The effective triggering of mitotic catastrophe in clinical practice requires induction of DNA damage as well as inhibition of the molecular pathways that regulate cell cycle arrest and DNA repair. Here we discuss various methods to detect mitotic catastrophe, the mechanisms of its development, and the attempts to use this phenomenon in cancer treatment.

PURPOSE: To compare the concentrations of interleukin (IL) (IL-1b, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12p70), interferon (IFN)-γ, tumor necrosis factor (TNF)-α, and TNF-β in the aqueous humor of patients undergoing femtosecond laser–assisted cataract surgery (FLACS) and corneal mechanical paracentesis treated with two different topical nonsteroidal anti-inflammatory drugs (NSAIDs): bromfenac and indomethacin. METHODS: In this prospective, randomized controlled, single-center study, aqueous humor samples were obtained immediately after performing the femtosecond laser procedure or at the start of conventional phacoemulsification. Preoperatively, the FLACS groups were administered (once daily and four times daily, respectively) either topical bromfenac 0.09% (12 eyes) or indomethacin 0.1% (12 eyes). The corneal paracentesis bromfenac and indomethacin groups received the same regimen of instillation of NSAIDs, respectively. Quantitative analysis of the expressed cytokines in the aqueous humor was performed using FlowCytomix FC 500 Pro 3.0 Software (Bender MedSystems GmbH, Vienna, Austria). RESULTS: The intraoperative pupil diameter was correlated with the expression of IL-6 after the femtosecond laser procedure in the FLACS indomethacin group (r = −0.53; P = .07). A significant difference in mean pupillary size was detected between the FLACS bromfenac and indomethacin groups at the aspiration/irrigation time point (0.53 ± 0.26 mm) and at the end of surgery (0.68 ± 0.37 mm). Progressive pupillary constriction was observed in the indomethacin and bromfenac groups. CONCLUSIONS: A smaller expression of IL-6 to the overall cytokine network value was observed in cases receiving preoperative bromfenac 0.09%, explaining improved maintenance of intraoperative mydriasis. [ J Refract Surg. 2018;34(10):646–652.]

Crohn's disease (CD) and ulcerative colitis (UC) are inflammatory bowel diseases (IBD) characterized by immune reactivity against microbial and auto-antigens. This work was designed to study the cytokine profile in blood serum and coproextracts of children with CD and UC. The studied patients consisted of 17 children with CD (group I), 17 children with UC (group II), and 18 controls with intestinal dysbiosis (group III). The diagnosis of UC and CD was based on accepted clinical and endoscopic criteria. The levels of 13 cytokines (IL-1β, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12p70, IL-17A, TNF-α, TGF-β, and IFN-γ) were determined in blood sera and coproextracts of the patients and controls using the BioPlex technology. The level of IL-17A was significantly increased and that of TGF-β was significantly decreased in the blood serum of the patients with IBDs. Changes in the cytokine profile in the coproextracts affected the wider spectrum of cytokines. The levels of proinflammatory cytokines (IL-2, IL-4, IL-6, IL-12p70, TNF-α, and IFN-γ) were increased 6-9-fold, whereas the level of the anti-inflammatory cytokine IL-10 was increased 3-fold. The cytokine balance was shifted to the proinflammatory cytokines. The TGF-β level was increased 9-fold and that of IL-17A was increased 3-fold. Thus, the cytokine profile in the coproextracts was more informative than that of the blood serum. The determination of cytokines in coproextracts is simple and noninvasive.

Lipopolysaccharide (LPS), a fragment of the bacterial cell wall, specifically interacting with protein complexes on the cell surface, can induce the production of pro-inflammatory and apoptotic signaling molecules, leading to the damage and death of brain cells. Similar effects have been noted in stroke and traumatic brain injury, when the leading factor of death is glutamate (Glu) excitotoxicity too. But being an amphiphilic molecule with a significant hydrophobic moiety and a large hydrophilic region, LPS can also non-specifically bind to the plasma membrane, altering its properties. In the present work, we studied the effect of LPS from Escherichia coli alone and in combination with the hyperstimulation of Glu-receptors on the functional state of mitochondria and Ca2+ homeostasis, oxygen consumption and the cell survival in primary cultures from the rats brain cerebellum and cortex. In both types of cultures, LPS (0.1–10 μg/ml) did not change the intracellular free Ca2+ concentration ([Ca2+]i) in resting neurons but slowed down the median of the decrease in [Ca2+]i on 14% and recovery of the mitochondrial potential (ΔΨm) after Glu removal. LPS did not affect the basal oxygen consumption rate (OCR) of cortical neurons; however, it did decrease the acute OCR during Glu and LPS coapplication. Evaluation of the cell culture survival using vital dyes and the MTT assay showed that LPS (10 μg/ml) and Glu (33 μM) reduced jointly and separately the proportion of live cortical neurons, but there was no synergism or additive action. LPS-effects was dependent on the type of culture, that may be related to both the properties of neurons and the different ratio between neurons and glial cells in cultures. The rapid manifestation of these effects may be the consequence of the direct effect of LPS on the rheological properties of the cell membrane.