Renal Collision Tumor: A Case of Small Cell Lung Cancer Metastasis to Renal Angiomyolipoma.

ABSTRACT: A 68-year-old woman presented with chest pain and shortness of breath. Imaging revealed a left hilar mass biopsy-proven as small cell cancer. Concurrently, a macroscopic fat-containing renal lesion consistent with an angiomyolipoma was observed. Systemic therapy achieved stability in the lungs and bones, and palliative radiation targeted the left hilum. However, progressive lung disease and brain metastases necessitated stereotactic radiosurgery for brain lesions. Notably, the renal angiomyolipoma exhibited increased soft tissue component and new focal uptake on FDG PET/CT. Biopsy confirmed metastatic small cell lung cancer within the renal lesion. This case highlights a rare occurrence of a renal collision tumor involving small cell cancer and angiomyolipoma.

Feasibility and safety of bipolar radiofrequency track cautery during percutaneous image-guided abdominal biopsy procedures.

PURPOSE: The purpose of this study was to assess the feasibility and safety of using a bipolar radiofrequency track cautery device during percutaneous image-guided abdominal biopsy procedures in at-risk patients. METHODS: Forty-two patients (26-79 years old; female 44%) with at least one bleeding risk factor who underwent an abdominal image-guided (CT or US) biopsy and intended bipolar radiofrequency track cautery (BRTC) were retrospectively studied. An 18G radiofrequency electrode was inserted through a 17G biopsy introducer needle immediately following coaxial 18G core biopsy, to cauterize the biopsy track using temperature control. Bleeding risk factors, technical success, and adverse events were recorded. RESULTS: BRTC was technically successful in 41/42 (98%) of procedures; in one patient, the introducer needle retracted from the liver due to respiratory motion prior to BRTC. BRTC following percutaneous biopsy was applied during 41 abdominal biopsy procedures (renal mass = 12, renal parenchyma = 10, liver mass = 9, liver parenchyma = 5, splenic mass or parenchyma = 4, gastrohepatic mass = 1). All patients had one or more of the following risk factors: high-risk organ (spleen or renal parenchyma), hypervascular mass, elevated prothrombin time, renal insufficiency, thrombocytopenia, recent anticoagulation or anticoagulation not withheld for recommended interval, cirrhosis, intraprocedural hypertension, brisk back bleeding observed from the introducer needle, or subcapsular tumor location. No severe adverse events (grade 3 or higher) occurred. Two (2/41, 5%) mild (grade 1) bleeding events did not cause symptoms or require intervention. CONCLUSION: Bipolar radiofrequency track cautery was feasible and safe during percutaneous image-guided abdominal biopsy procedures. IRB approval: MBG 2022P002277.

Quantifying Impact of Disruption to Radiology Education During the COVID-19 Pandemic and Implications for Future Training.

PURPOSE: The aim of this study was to assess the impact on radiology resident education due to the COVID-19 pandemic in order to inform future educational planning. METHODS: During a 10-week study period from March 16 to May 22, 2020, changes to educational block-weeks (BW) of first through fourth year residents (R1-4) were documented as disrupted in the setting of the COVID-19 pandemic. The first 5 weeks and the second 5 weeks were evaluated separately for temporal differences. Overall and mean disrupted BW per resident were documented. Wilcoxon rank-sum tests were used to assess pairwise differences between classes with Bonferroni-adjusted P-values, as well as differences in the early versus later phase of the pandemic. RESULTS: Of 373 BW, 56.6% were assigned to virtual curriculum, 39.4% radiology clinical duties, 2.9% illness, and 1.1% reassignment. Scheduling intervention affected 6.2 ± 2.3 (range 1-10) mean BW per resident over the 10-week study period. The R3 class experienced the largest disruption, greater than the R2 classes, and statistically significantly more than the R1 and R4 classes (both P < 0.05). The second half of the pandemic caused statistically significantly more schedule disruptions than the first half (P = 0.009). DISCUSSION: The impact of COVID-19 pandemic varied by residency class year, with the largest disruption of the R3 class and the least disruption of the R4 class. To optimize future educational opportunities, shifting to a competency-based education paradigm may help to achieve proficiency without extending the length of the training program.

Beyond business as usual: Radiology residency educational response to the COVID-2019 pandemic.

The COVID-19 pandemic has disrupted standard hospital operations and diagnostic radiology resident education at academic medical centers across the country. Deferment of elective surgeries and procedures coupled with a shift of resources toward increased inpatient clinical needs for the care of COVID-19 patients has resulted in substantially decreased imaging examinations at many institutions. Additionally, both infection control and risk mitigation measures have resulted in minimal on-site staffing of both trainees and staff radiologists at many institutions. As a result, residents have been placed in nonstandard learning environments, including working from home, engaging in a virtual curriculum, and participating in training sessions in preparation for potential reassignment to other patient care settings. Typically, for residents to gain the necessary knowledge, skills, and experience to practice independently upon graduation, radiology training programs must provide an optimal balance between resident education and clinical obligations. We describe our experience adapting to the challenges in educational interruptions and clinical work reassignments of 41 interventional and diagnostic radiology residents at a large academic center. We highlight opportunities for collaboration and teamwork in creatively adjusting and planning for the short and long-term impact of the pandemic on resident education. This experience shows how the residency educational paradigm was shifted during a pandemic and can serve as a template to address future disruptions.

Vascular imaging in renal donors.

Imaging plays a crucial role in pre-transplant evaluation to enhance the probability of a successful outcome. Its aim is to define kidney and vascular anatomy and to assess potential pathologies. Each modality has advantages and disadvantages. Computed tomography angiography (CTA) is the most commonly used imaging modality, however, magnetic resonance angiography (MRA) can be used in selected cases. The purpose of this review article is to provide an overview of available imaging modalities, their benefits, risks, advantages, and disadvantages. Imaging findings that indicate particular anomalies and pathologies that may affect living renal donor selection will be discussed.

Opposite rheological properties of neuronal microcompartments predict axonal vulnerability in brain injury.

Although pathological changes in axonal morphology have emerged as important features of traumatic brain injury (TBI), the mechanical vulnerability of the axonal microcompartment relative to the cell body is not well understood. We hypothesized that soma and neurite microcompartments exhibit distinct mechanical behaviors, rendering axons more sensitive to a mechanical injury. In order to test this assumption, we combined protein micropatterns with magnetic tweezer rheology to probe the viscoelastic properties of neuronal microcompartments. Creep experiments revealed two opposite rheological behaviors within cortical neurons: the cell body was soft and characterized by a solid-like response, whereas the neurite compartment was stiffer and viscous-like. By using pharmacological agents, we demonstrated that the nucleus is responsible for the solid-like behavior and the stress-stiffening response of the soma, whereas neurofilaments have a predominant contribution in the viscous behavior of the neurite. Furthermore, we found that the neurite is a mechanosensitive compartment that becomes softer and adopts a pronounced viscous state on soft matrices. Together, these findings highlight the importance of the regionalization of mechanical and rigidity-sensing properties within neuron microcompartments in the preferential damage of axons during traumatic brain injury and into potential mechanisms of axonal outgrowth after injury.

Traumatic brain injury and the neuronal microenvironment: a potential role for neuropathological mechanotransduction.

Traumatic brain injury (TBI) is linked to several pathologies for which there is a lack of understanding of disease mechanisms and therapeutic strategies. To elucidate injury mechanisms, it is important to consider how physical forces are transmitted and transduced across all spatial scales of the brain. Although the mechanical response of the brain is typically characterized by its material properties and biological structure, cellular mechanotransduction mechanisms also exist. Such mechanisms can affect physiological processes by responding to exogenous mechanical forces directed through sub-cellular components, such as extracellular matrix and cell adhesion molecules, to mechanosensitive intracellular structures that regulate mechanochemical signaling pathways. We suggest that cellular mechanotransduction may be an important mechanism underlying the initiation of cell and sub-cellular injuries ultimately responsible for the diffuse pathological damage and clinical symptoms observed in TBI, thereby providing potential therapeutic opportunities not previously explored in TBI.

Three-dimensional paper-based model for cardiac ischemia.

In vitro models of ischemia have not historically recapitulated the cellular interactions and gradients of molecules that occur in a 3D tissue. This work demonstrates a paper-based 3D culture system that mimics some of the interactions that occur among populations of cells in the heart during ischemia. Multiple layers of paper containing cells, suspended in hydrogels, are stacked to form a layered 3D model of a tissue. Mass transport of oxygen and glucose into this 3D system can be modulated to induce an ischemic environment in the bottom layers of the stack. This ischemic stress induces cardiomyocytes at the bottom of the stack to secrete chemokines which subsequently trigger fibroblasts residing in adjacent layers to migrate toward the ischemic region. This work demonstrates the usefulness of patterned, stacked paper for performing in vitro mechanistic studies of cellular motility and viability within a model of the laminar ventricle tissue of the heart.

A potential role for integrin signaling in mechanoelectrical feedback.

Certain forms of heart disease involve gross morphological changes to the myocardium that alter its hemodynamic loading conditions. These changes can ultimately lead to the increased deposition of extracellular matrix (ECM) proteins, such as collagen and fibronectin, which together work to pathologically alter the myocardium's bulk tissue mechanics. In addition to changing the mechanical properties of the heart, this maladaptive remodeling gives rise to changes in myocardium electrical conductivity and synchrony since the tissue's mechanical properties are intimately tied to its electrical characteristics. This phenomenon, called mechanoelectrical coupling (MEC), can render individuals affected by heart disease arrhythmogenic and susceptible to Sudden Cardiac Death (SCD). The underlying mechanisms of MEC have been attributed to various processes, including the action of stretch activated channels and changes in troponin C-Ca(2+) binding affinity. However, changes in the heart post infarction or due to congenital myopathies are also accompanied by shifts in the expression of various molecular components of cardiomyocytes, including the mechanosensitive family of integrin proteins. As transmembrane proteins, integrins mechanically couple the ECM with the intracellular cytoskeleton and have been implicated in mediating ion homeostasis in various cell types, including neurons and smooth muscle. Given evidence of altered integrin expression in the setting of heart disease coupled with the associated increased risk for arrhythmia, we argue in this review that integrin signaling contributes to MEC. In light of the significant mortality associated with arrhythmia and SCD, close examination of all culpable mechanisms, including integrin-mediated MEC, is necessary.

Blast-induced phenotypic switching in cerebral vasospasm.

Vasospasm of the cerebrovasculature is a common manifestation of blast-induced traumatic brain injury (bTBI) reported among combat casualties in the conflicts in Afghanistan and Iraq. Cerebral vasospasm occurs more frequently, and with earlier onset, in bTBI patients than in patients with other TBI injury modes, such as blunt force trauma. Though vasospasm is usually associated with the presence of subarachnoid hemorrhage (SAH), SAH is not required for vasospasm in bTBI, which suggests that the unique mechanics of blast injury could potentiate vasospasm onset, accounting for the increased incidence. Here, using theoretical and in vitro models, we show that a single rapid mechanical insult can induce vascular hypercontractility and remodeling, indicative of vasospasm initiation. We employed high-velocity stretching of engineered arterial lamellae to simulate the mechanical forces of a blast pulse on the vasculature. An hour after a simulated blast, injured tissues displayed altered intracellular calcium dynamics leading to hypersensitivity to contractile stimulus with endothelin-1. One day after simulated blast, tissues exhibited blast force dependent prolonged hypercontraction and vascular smooth muscle phenotype switching, indicative of remodeling. These results suggest that an acute, blast-like injury is sufficient to induce a hypercontraction-induced genetic switch that potentiates vascular remodeling, and cerebral vasospasm, in bTBI patients.

A possible role for integrin signaling in diffuse axonal injury.

Over the past decade, investigators have attempted to establish the pathophysiological mechanisms by which non-penetrating injuries damage the brain. Several studies have implicated either membrane poration or ion channel dysfunction pursuant to neuronal cell death as the primary mechanism of injury. We hypothesized that traumatic stimulation of integrins may be an important etiological contributor to mild Traumatic Brain Injury. In order to study the effects of forces at the cellular level, we utilized two hierarchical, in vitro systems to mimic traumatic injury to rat cortical neurons: a high velocity stretcher and a magnetic tweezer system. In one system, we controlled focal adhesion formation in neurons cultured on a stretchable substrate loaded with an abrupt, one dimensional strain. With the second system, we used magnetic tweezers to directly simulate the abrupt injury forces endured by a focal adhesion on the neurite. Both systems revealed variations in the rate and nature of neuronal injury as a function of focal adhesion density and direct integrin stimulation without membrane poration. Pharmacological inhibition of calpains did not mitigate the injury yet the inhibition of Rho-kinase immediately after injury reduced axonal injury. These data suggest that integrin-mediated activation of Rho may be a contributor to the diffuse axonal injury reported in mild Traumatic Brain Injury.