Two of the classical hallmarks of cancer are uncontrolled cell division and tissue invasion, which turn the disease into a systemic, life-threatening condition. Although both processes are studied, a clear correlation between cell division and motility of cancer cells has not been described previously. Here, we experimentally characterize the dynamics of invasive and non-invasive breast cancer tissues using human and murine model systems. The intrinsic tissue velocities, as well as the divergence and vorticity around a dividing cell correlate strongly with the invasive potential of the tissue, thus showing a distinct correlation between tissue dynamics and aggressiveness. We formulate a model which treats the tissue as a visco-elastic continuum. This model provides a valid reproduction of the cancerous tissue dynamics, thus, biological signaling is not needed to explain the observed tissue dynamics. The model returns the characteristic force exerted by an invading cell and reveals a strong correlation between force and invasiveness of breast cancer cells, thus pinpointing the importance of mechanics for cancer invasion.

Mechanical forces are important factors in the development, coordination and collective motion of cells. Based on a continuum-scale model, we consider the influence of substrate friction on cell motility in confluent living tissue. We test our model on the experimental data of endothelial and cancer cells. In contrast to the commonly used drag friction, we find that solid friction best captures the cell speed distribution. From our model, we quantify a number of measurable physical tissue parameters, such as the ratio between the viscosity and substrate friction.

Many natural fracture systems are characterized by a single length scale, which is the distance between neighboring fractures. Examples are mud cracks and columnar jointing. In columnar jointing the origin of this scale has been a long‐standing issue. Here we present a comprehensive study of columnar jointing based on experiments on cooling stearic acids, numerical simulations using both discrete and finite element methods and basic analytical calculations. We show that the diameter of columnar joints is a nontrivial function of the material properties and the cooling conditions of the system. We determine the shape of this function analytically and show that it is in agreement with the experiments and the numerical simulations.

Background Severe shoulder pain occurs frequently after surgery close to the diaphragm, potentially caused by referred pain via the ipsilateral phrenic nerve. We aimed to assess the analgesic effect of an ultrasound‐guided phrenic nerve block on moderate to severe right‐sided shoulder pain after open partial hepatectomy. Methods This was a randomized, double‐blind, placebo‐controlled, pilot study, comparing ultrasound‐guided phrenic nerve block (ropivacaine 0.75 mg/mL) versus placebo (isotonic sodium chloride 0.9 mg/mL) on severe post‐hepatectomy shoulder pain (NRS ≥6). Pre‐ and postoperative spirometry and arterial blood gas analyses were used to assess respiratory function. Subjects with chronic lung disease were excluded. Unfortunately, due to lack of funding, the trial was ended prematurely and therefore presented as a pilot study. Results One hundred and one subjects were screened for eligibility; 14 subjects were randomized, and two subjects were later excluded; thus, 12 subjects were analyzed with six in each group. A statistically significant difference in reduction in median pain intensity between groups was observed 15 minutes after phrenic nerve block (“ropivacaine first” ΔNRS: −6.0 [−6.0 to −3.0] vs. “saline first” ΔNRS: 0 [−6.0 to 1.0], P = .026). Spirometry results and arterial blood gas analyses were not clinically impacted by the block. Conclusions Postoperative phrenic nerve block significantly reduced severe post‐hepatectomy shoulder pain. Larger studies are warranted to confirm the lack of clinically relevant block‐related impairment of respiratory function.

The aim of this study was to characterize the clinical signs and symptoms of exposures to aripiprazole overdoses. We retrospectively identified all aripiprazole exposures reported to the Danish Poison Information Centre (DPIC) from June 2007 to May 2015. Information concerning demographics, ingested dose and symptoms was extracted from the DPIC database and medical records. Information on death and admission to hospital was obtained from Danish national registers. We analysed 239 cases, 86 concerning single-drug exposures to aripiprazole, and 153 cases where aripiprazole had been taken with at least one other substance (mixed-drug). The median ingested aripiprazole dose was 105 mg (IQR: 50-1680 mg) in the single-drug exposure group and 120 mg (IQR: 60-225 mg) in the mixed-drug exposure group. The most commonly reported symptom was light sedation, reported in 63% of the single-drug group and 50% of the mixed-drug exposure group. There were no malignant arrhythmias or ECG abnormalities after single-drug exposures. No deaths were recorded in relation to the intake. We found a long-term mortality rate of 13 deaths per 1000 person-years (95% CI: 7; 23 per 1000 person-years), which is significantly higher than in an age- and gender-matched background population. In conclusion, we found that aripiprazole overdoses had few and mild symptoms predominantly related to the sedative properties. We detected a benign cardiovascular safety profile and no new safety concerns. Our findings may support an increased threshold of 300 mg for hospital admission after a single-drug exposure with aripiprazole and symptoms not worse than light sedation.