We study coagulation equations under non-equilibrium conditions which are induced by the addition of a source term for small cluster sizes. We consider both discrete and continuous coagulation equations, and allow for a large class of coagulation rate kernels, with the main restriction being boundedness from above and below by certain weight functions. The weight functions depend on two power law parameters, and the assumptions cover, in particular, the commonly used free molecular and diffusion limited aggregation coagulation kernels. Our main result shows that the two weight function parameters already determine whether there exists a stationary solution under the presence of a source term. In particular, we find that the diffusive kernel allows for the existence of stationary solutions while there cannot be any such solutions for the free molecular kernel. The argument to prove the non-existence of solutions relies on a novel power law lower bound, valid in the appropriate parameter regime, for the decay of stationary solutions with a constant flux. We obtain optimal lower and upper estimates of the solutions for large cluster sizes, and prove that the solutions of the discrete model behave asymptotically as solutions of the continuous model.

We study coagulation equations under non-equilibrium conditions which are induced by the addition of a source term for small cluster sizes. We consider both discrete and continuous coagulation equations, and allow for a large class of coagulation rate kernels, with the main restriction being boundedness from above and below by certain weight functions. The weight functions depend on two power law parameters, and the assumptions cover, in particular, the commonly used free molecular and diffusion limited aggregation coagulation kernels. Our main result shows that the two weight function parameters already determine whether there exists a stationary solution under the presence of a source term. In particular, we find that the diffusive kernel allows for the existence of stationary solutions while there cannot be any such solutions for the free molecular kernel. The argument to prove the non-existence of solutions relies on a novel power law lower bound, valid in the appropriate parameter regime, for the decay of stationary solutions with a constant flux. We obtain optimal lower and upper estimates of the solutions for large cluster sizes, and prove that the solutions of the discrete model behave asymptotically as solutions of the continuous model. 7 Convergence of discrete to continuous model * K (x, y) ≥ c 1 x γ+λ y −λ + y γ+λ x −λ , (2.11)

Gender-affirming surgeries expand the options for physical transition among transgender patients, those whose gender identity is incongruent with the sex assigned to them at birth. Growing medical insight, increasing public acceptance, and expanding insurance coverage have improved the access to and increased the demand for gender-affirming surgeries in the United States. Procedures for transgender women, those patients with feminine gender identity, include breast augmentation using implants and genital reconstruction with vaginoplasty. Some transgender women receive medically unapproved silicone injections for breast augmentation or other softtissue contouring procedures that can lead to disfigurement, silicone pulmonary embolism, systemic reactions, and even death. MRI is preferred over CT for postvaginoplasty evaluation given its superior tissue contrast resolution. Procedures for transgender men, patients with a masculine gender identity, include chest masculinization (mastectomy) and genital reconstruction (phalloplasty or metoidioplasty, scrotoplasty, and erectile device implantation). Urethrography is the standard imaging modality performed to evaluate neourethral patency and other complications, such as leaks and fistulas. Despite a sizeable growth in the surgical literature about gender-affirming surgeries and their outcomes, detailed descriptions of the imaging features following these surgeries remain sparse. Radiologists must be aware of the wide variety of anatomic and pathologic changes unique to patients who undergo gender-affirming surgeries to ensure accurate imaging interpretation.

Pseudostratified epithelia (PSE) are a common type of columnar epithelia found in a wealth of embryonic and adult tissues such as ectodermal placodes, the trachea, the ureter, the gut and the neuroepithelium. PSE are characterized by the choreographed displacement of cells' nuclei along the apicobasal axis according to phases of their cell cycle. Such movements, called interkinetic movements (INM), have been proposed to influence tissue expansion and shape and suggested as culprit in several congenital diseases such as CAKUT (Congenital anomalies of kidney and urinary tract) and esophageal atresia. INM rely on cytoskeleton dynamics just as adhesion, contractility and mitosis do. Therefore, long term impairment of INM without affecting proliferation and adhesion is currently technically unachievable. Here we bypassed this hurdle by generating a 2D agent-based model of a proliferating PSE and compared its output to the growth of the chick neuroepithelium to assess the interplay between INM and these other important cell processes during growth of a PSE. We found that INM directly generates apical expansion and apical nuclear crowding. In addition, our data strongly suggest that apicobasal elongation of cells is not an emerging property of a proliferative PSE but rather requires a specific elongation program. We then discuss how such program might functionally link INM, tissue growth and differentiation. Author summaryPseudostratified epithelia (PSE) are a common type of epithelia characterized by the choreographed displacement of cells' nuclei along the apicobasal axis during proliferation. These so-called interkinetic movements (INM) were proposed to influence tissue expansion and suggested as culprit in several congenital diseases. INM rely on cytoskeleton dynamics. Therefore, longer term impairment of INM without affecting proliferation and adhesion is currently technically unachievable. We bypassed this hurdle by generating a mathematical model of PSE and compared it to the growth of an epithelium of reference.Our data show that INM drive expansion of the apical domain of the epithelium and suggest that apicobasal elongation of cells is not an emerging property of a proliferative PSE but might rather requires a specific elongation program.Interkinetic movements impact the growth of pseudostratified epithelia PLOS Computational Biology | https://doi.