Several human studies indicate that mobile phone specific electromagnetic fields may cause cancer in humans but the underlying molecular mechanisms are currently not known. Studies concerning chromosomal damage (which is causally related to cancer induction) are controversial and those addressing this issue in mobile phone users are based on the use of questionnaires to assess the exposure. We realized the first human intervention trial in which chromosomal damage and acute toxic effects were studied under controlled conditions. The participants were exposed via headsets at one randomly assigned side of the head to low and high doses of a UMTS signal (n = 20, to 0.1 W/kg and n = 21 to 1.6 W/kg Specific Absorption Rate) for 2 h on 5 consecutive days. Before and three weeks after the exposure, buccal cells were collected from both cheeks and micronuclei (MN, which are formed as a consequence of structural and numerical chromosomal aberrations) and other nuclear anomalies reflecting mitotic disturbance and acute cytotoxic effects were scored. We found no evidence for induction of MN and of nuclear buds which are caused by gene amplifications, but a significant increase of binucleated cells which are formed as a consequence of disturbed cell divisions, and of karyolitic cells, which are indicative for cell death. No such effects were seen in cells from the less exposed side. Our findings indicate that mobile phone specific high frequency electromagnetic fields do not cause acute chromosomal damage in oral mucosa cells under the present experimental conditions. However, we found clear evidence for disturbance of the cell cycle and cytotoxicity. These effects may play a causal role in the induction of adverse long term health effects in humans.

Cytokinesis of animal and fungi cells depends crucially on the anillin scaffold proteins. Fission yeast anillin-related Mid1 anchors cytokinetic ring precursor nodes to the membrane. However, it is unclear if both of its Pleckstrin Homology (PH) and C2 C-terminal domains bind to the membrane as monomers or dimers, and if one domain plays a dominant role. We studied Mid1 membrane binding with all-atom molecular dynamics near a membrane with yeast-like lipid composition. In simulations with the full C terminal region started away from the membrane, Mid1 binds through the disordered L3 loop of C2 in a vertical orientation, with the PH away from the membrane. However, a configuration with both C2 and PH initially bound to the membrane remains associated with the membrane. Simulations of C2-PH dimers show extensive asymmetric membrane contacts. These multiple modes of binding may reflect Mid1\'s multiple interactions with membranes, node proteins, and ability to sustain mechanical forces.

Most cells can sense and change their shape to carry out fundamental cell processes. In many eukaryotes, the septin cytoskeleton is an integral component in coordinating shape changes like cytokinesis, polarized growth, and migration. Septins are filament-forming proteins that assemble to form diverse higher-order structures and, in many cases, are found in different areas of the plasma membrane, most notably in regions of micron-scale positive curvature. Monitoring the process of septin assembly in vivo is hindered by the limitations of light microscopy in cells, as well as the complexity of interactions with both membranes and cytoskeletal elements, making it difficult to quantify septin dynamics in living systems. Fortunately, there has been substantial progress in the past decade in reconstituting the septin cytoskeleton in a cell-free system to dissect the mechanisms controlling septin assembly at high spatial and temporal resolutions. The core steps of septin assembly include septin heterooligomer association and dissociation with the membrane, polymerization into filaments, and the formation of higher-order structures through interactions between filaments. Here, we present three methods to observe septin assembly in different contexts: planar bilayers, spherical supports, and rod supports. These methods can be used to determine the biophysical parameters of septins at different stages of assembly: as single octamers binding the membrane, as filaments, and as assemblies of filaments. We use these parameters paired with measurements of curvature sampling and preferential adsorption to understand how curvature sensing operates at a variety of length and time scales.

Anzer honey is well known in Turkey and used for its medicinal properties, especially for pharyngitis, tonsillitis, ulcers and cancer. In this study, we investigated whether Anzer honey, which is shown to have antioxidant, anti-tumoral, and anti-inflammatory properties, has a protective effect against X-ray induced genotoxic damage by cytogenetic methods. Peripheral blood lymphocytes isolated from 20 healthy volunteers were divided into two groups and cultivated by conventional methods. Study group lymphocytes were treated with 10% diluted honey while those in the control group were not. Both groups were exposed to a high dose (2 Gy) X-ray at the 48th hour of culture. Conventional cytogenetic staining and Giemsa banding methods were applied to evaluate chromosomal breakage and ring formation. Micronucleus frequencies were determined by the cytokinesis-block micronucleus (CBMN) assay. Paired sample t test was used to compare groups. Anzer honey, which was analyzed melissopalynologically, was used. Micronucleus frequency was significantly decreased in the study group (CI = 348.75 ± 31, median 326, min. 98, max. 704) compared to the control group (CI = 489.10 ± 27, median 500, min. 216, max. 645) (p = .001). Chromosomal breakage was also significantly decreased in the study group (CI = 118.70 ± 16, median 109, min. 12, max. 316) compared to the control group (CI = 233.60 ± 25, median 225, min. 65, max. 492) (p < .0001). This is the first study indicating that genotoxic damage in the peripheral blood lymphocytes of healthy volunteers induced by X-radiation may be prevented or alleviated by adding Anzer honey in vitro. These results encourage further research about the protective effects of honey. RESEARCH HIGHLIGHTS: Anzer honey has a genoprotective effect against radiation-induced genotoxicity, probably by preventing oxidation damage.

To analyze the effects of different anaesthetic methods on perioperative cellular immunity and long-term outcome in patients who undergo esophageal cancer surgery.
METHODS: A total of 120 patients with esophageal cancer admitted to Zhengzhou University People\'s Hospital from January 2016 to January 2017 were recruited and randomly divided into a GA group (general anaesthesia, n = 40), a PG group (paravertebral nerve block with general anaesthesia, n = 40) and an EG group (epidural anaesthesia with general anaesthesia, n = 40).
METHODS: Self-rating anxiety scale and visual analogue scale scores were adopted to compare postoperative anxiety and the degree of pain of patients in the three groups. In addition, the adverse reactions of patients in the three groups were compared. The levels of interleukin-6 (IL-6), IL-4, tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), and the survival of T-cell subsets (CD3+, CD4+, CD8+, CD4+/CD8+) before operation, at the end of operation, and on postoperative day (POD) 1 and POD 2 were measured by either ELISA or flow cytometry.
RESULTS: In the PG and EG group, the VAS scores were lower, and fewer opioids and vasoactive agents were used than in the GA group. In both the EG and PG groups, higher CD3+ and CD4+ cell survival and lower levels of Cor, IL-4, and IL-6 were identified at the end of or after the surgery than in the GA group. Moreover, the postoperative survival curves of the PG and EG groups were better than that of the GA group.
CONCLUSIONS: The combination of paravertebral nerve block or epidural anaesthesia and general anaesthesia may improve perioperative immune function and long-term outcome in patients who undergo esophageal cancer surgery.

Cytokinesis is required to cleave the daughter cells at the end of mitosis and relies on the spatiotemporal control of RhoA GTPase. Cytokinesis failure can lead to changes in cell fate or aneuploidy, which can be detrimental during development and/or can lead to cancer. However, our knowledge of the pathways that regulate RhoA during cytokinesis is limited, and the role of other Rho family GTPases is not clear. This is largely because the study of Rho GTPases presents unique challenges using traditional cell biological and biochemical methods, and they have pleiotropic functions making genetic studies difficult to interpret. The recent generation of optogenetic tools and biosensors that control and detect active Rho has overcome some of these challenges and is helping to elucidate the role of RhoA in cytokinesis. However, improvements are needed to reveal the role of other Rho GTPases in cytokinesis, and to identify the molecular mechanisms that control Rho activity. This review examines some of the outstanding questions in cytokinesis, and explores tools for the imaging and control of Rho GTPases.

Perturbation of epigenetic regulation is a well-established mechanism for cancer but its role for lead (Pb)-associated toxicity has not been adequately investigated. We aimed to investigate whether occupational Pb exposure is associated with micronuclei (MN) frequency and to further explored the mediating roles of epigenetic gene regulation. All the Pb-exposed workers recruited from a Chinese acid battery factory, blood lead levels (BLLs) and MN frequency in lymphocytes were measured. In addition, methylation levels of seven genes (Line-1, RASSF1A, RUNX3, p16, CYP26C1, hMLH1, p15) were examined among 230 workers. Robust Poisson regression model was used to investigate the association between BLLs and MN frequency. Mediation analysis was used to explore the mediating role of specific DNA methylation. Among total 677 participants, 71% were male, median BLLs was 229.1 μg/L (P25  = 155.5, P75  = 319.3; ranged from 8.9 to 647.7 μg/L), mean MN frequency was 2.5‰ (SD = 1.8‰; ranged from 0 to 9‰). Results from base model, adjusted for age, sex, and body mass index, showed that MN frequency would increase 1.38 (95%confidential interval: 1.34, 1.43) per 100 μg/L increment in BLLs. Using categorized exposure variable analyses, a BLLs dose-response increase in MN frequency was observed: 2.74 (2.13, 3.51), 3.43 (2.73, 4.32), 4.41 (3.89, 5.01) to 6.86 (6.02, 7.81). Mediation analysis indicated that Line-1 methylation significantly mediated 3.6% of the association of BLLs with MN frequency. Occupational Pb exposure induces MN frequency in a dose-response relationship. Part of this association was mediated by Line-1 promotor methylation.

Cytokinesis is the process that separates a cell into two daughter cells at the end of mitosis. Most of our knowledge of cytokinesis comes from overexpression studies, which affects our interpretation of protein function. Gene editing can circumvent this issue by introducing functional mutations or fluorescent probes directly into a gene locus. However, despite its potential, gene editing is just starting to be used in the field of cytokinesis. Here, we discuss the benefits of using gene editing tools for the study of cytokinesis and highlight recent studies that successfully used CRISPR-Cas (clustered regularly interspaced short palindromic repeats-CRISPR-associated proteins) technology to answer critical questions regarding the function of cytokinesis proteins. We also present methodologies for editing essential genes and discuss how CRISPR interference (CRISPRi) and activation (CRISPRa) can enable precise control of gene expression to answer important questions in the field. Finally, we address the need for gene editing to study cytokinesis in more physiologically relevant contexts. Therefore, this Review provides a roadmap for gene editing to be used in the study of cytokinesis and other cellular processes.

Radiopharmaceuticals are special medicines composed by a radionuclide and a non-radioactive compound characterized by non-pharmacodynamic effects, low prevalence of side effects, and a possible risk of oncogenesis, since its administration to patients supposes a radiation dose to organism. Over these years, radiation damage induced by diagnosis radiopharmaceuticals has been evaluated, including the radiolabeled autologous cells, a group of radiopharmaceuticals where blood cells extracted from patients are labeled in-vitro and readministered for diagnosis. There is not a consensus about the possibility of increasement of risk for malignancies associated with the radiolabeled blood cells, so for a more accurate evaluation of the potential oncogenic risk related to the administration of [Tc]Tc labeled red blood cells, radiation dose received by the cells during the labeling process is studied by means of the cytokinesis-blocked micronucleus (CBMN) assay and a dose-response curve constructed by in-vitro external irradiation of blood samples. Our work enables to establish the range of activity to be added during the in-vitro labeling of red blood cells with [Tc]Tc pertechnetate to avoid radiation damage to cells. Activities recommended for blood volume determination and angiography do not increase the risk of malignancies, whilst activities of 370 MBq show chromosome aberrations in lymphocytes. Evaluation of the radiation damage related to the in-vitro labeling is recommended to estimate the potential oncogenic risk and minimize it.

Cytokinesis is the process that completes cell division by partitioning the contents of the mother cell between the two daughter cells. It involves the highly regulated assembly and constriction of an actomyosin contractile ring, whose function is to pinch the mother cell in two. Research on the contractile ring has particularly focused on the signaling mechanisms that dictate when and where the ring is formed. In vivo studies of ring constriction are however scarce and its mechanistic understanding is therefore limited. Here we present several experimental approaches for monitoring ring constriction in vivo, using the four-cell C. elegans embryo as model. These approaches allow for the ring to be perturbed only after it forms and include the combination of live imaging with acute drug treatments, temperature-sensitive mutants and rapid temperature shifts, as well as laser microsurgery. In addition, we explain how to combine these with RNAi-mediated depletion of specific components of the cytokinetic machinery.