Planktos: An Agent-Based Modeling Framework for Small Organism Movement and Dispersal in a Fluid Environment with Immersed Structures.

Multiscale modeling of marine and aerial plankton has traditionally been difficult to address holistically due to the challenge of resolving individual locomotion dynamics while being carried with larger-scale flows. However, such problems are of paramount importance, e.g., dispersal of marine larval plankton is critical for the health of coral reefs, and aerial plankton (tiny arthropods) can be used as effective agricultural biocontrol agents. Here we introduce the open-source, agent-based modeling software Planktos targeted at 2D and 3D fluid environments in Python. Agents in this modeling framework are relatively tiny organisms in sufficiently low densities that their effect on the surrounding fluid motion can be considered negligible. This library can be used for scientific exploration and quantification of collective and emergent behavior, including interaction with immersed structures. In this paper, we detail the implementation and functionality of the library along with some illustrative examples. Functionality includes arbitrary agent behavior obeying either ordinary differential equations, stochastic differential equations, or coded movement algorithms, all under the influence of time-dependent fluid velocity fields generated by computational fluid dynamics, experiments, or analytical models in domains with static immersed mesh structures with sliding or sticky collisions. In addition, data visualization tools provide images or animations with kernel density estimation and velocity field analysis with respect to deterministic agent behavior via the finite-time Lyapunov exponent.

Abscesses due to mycobacterium abscessus linked to injection of unapproved alternative medication.

An unlicensed injectable medicine sold as adrenal cortex extract (ACE*) and distributed in the alternative medicine community led to the largest outbreak of Mycobacterium abscessus infections reported in the United States. Records from the implicated distributor from January 1, 1995, to August 18, 1996, were used to identify purchasers; purchasers and public health alerts were used to identify patients. Purchasers and patients were interviewed, and available medical records were reviewed. Vials of ACE* were tested for mycobacterial contamination, and the product was recalled by the U.S. Food and Drug Administration. ACE* had been distributed to 148 purchasers in 30 states; 87 persons with postinjection abscesses attributable to the product were identified. Patient and vial cultures contained M. abscessus identical by enzymatic and molecular typing methods. Unusual infectious agents and alternative health practices should be considered in the diagnosis of infections that do not respond to routine treatment.

Inhibition of epidermal growth factor-like growth factor secretion in tracheobronchial epithelial cells by vitamin A.

Vitamin A deficiency of respiratory tract epithelium results in the phenomenon of squamous cell metaplasia. The mechanisms by which vitamin A regulates airway epithelial cell growth and differentiation are not completely understood. In this study, we focused on the effects of vitamin A (retinol) on growth of human and non-human primate tracheobronchial epithelial (TBE) cells in culture. Retinol and its derivatives have little growth-stimulatory effect on TBE cells that are maintained in primary culture in a serum-free medium supplemented with 6 hormonal supplements: insulin, transferrin, epidermal growth factor (EGF), hydrocortisone, cholera toxin, and bovine hypothalamus extract. However, it was observed that retinol exhibited dose-dependent inhibition of TBE cell growth when EGF was removed from this serum-free culture condition. This inhibition can be reversed if EGF or the conditioned medium of primary TBE cells that are maintained in vitamin A-deficient condition is added. This type of EGF-retinol interacting phenomenon was not observed with the 5 remaining hormonal supplements. Analysis of 125I-labeled EGF binding shows a down-regulation of the high affinity binding sites (Kd = 0.09 nM) on TBE cells grown in the absence of vitamin A. These results suggest that TBE cells are capable of secreting an EGF-like growth factor in the absence of vitamin A. The possibility that transforming growth factor-alpha (TGF-alpha) is involved in this phenomenon is further examined by antibodies specific to TGF-alpha and its binding to an EGF-receptor. Using the TGF-alpha antibody, the presence of a TGF-alpha-specific antigen was found to be 3-fold higher in the conditioned medium obtained from the vitamin A-deficient cultures than that derived from retinol-treated cultures. Furthermore, the antibody neutralizing the TGF-alpha binding to an EGF receptor was able to reduce the DNA synthesis associated with the vitamin A deficiency. These results suggest that vitamin A plays an important regulatory role in the paracrine/autocrine secretion of EGF/TGF-alpha-like mitogen in TBE cell cultures.