Radiology Resident Ownership Scale (RROS): Adapting a Validated Measure of Patient Care Ownership to the Radiology Context.

RATIONALE AND OBJECTIVES: The aim of this study was to develop a validated instrument to measure radiology residents' sense of psychological ownership of patient care. MATERIALS AND METHODS: A previously validated measure of patient care ownership was adapted through a two-step process of expert review and revision by six academic radiology faculty. An online, anonymous survey was distributed to 64 residents and fellows at the end of three consecutive four-week long rotations. We calculated Cronbach's α to determine the scale's internal consistency, performed exploratory factor analysis to identify possible subscales, and conducted bivariate and correlational analysis to establish construct validity. RESULTS: The 11-item ownership scale demonstrated good internal consistency (Cronbach's α = 0.93), and three subscales were identified corresponding to assertiveness, conscientiousness, and confidence/perceived competence. Sense of ownership was significantly associated with training level, prior experience in the type of rotation, stress, sleep, burnout, peer support, relationships with clinical staff, and recognition by department. We found no significant association between ownership and age, gender, type of rotation, site of rotation, type of residency, perceived interruption frequency, or remote work frequency. CONCLUSION: The radiology resident patient care ownership scale demonstrates good internal consistency and preliminary evidence of validity. After further validation, we expect the scale to be a valuable tool in evaluating interventions aimed at increasing radiology residents' sense of ownership.

Body Imaging of Bacterial and Parasitic Zoonoses: Keys to Diagnosis.

Zoonotic infections, which are transmitted from animals to humans, have been a substantial source of human disease since antiquity. As the human population continues to grow and human influence on the planet expands, humans frequently encounter both domestic and wild animals. This has only increased as deforestation, urbanization, agriculture, habitat fragmentation, outdoor recreation, and international travel evolve in modern society, all of which have resulted in the emergence and reemergence of zoonotic infections. Zoonotic infections pose a diagnostic challenge because of their nonspecific clinical manifestations and the need for specialized testing procedures to confirm these diagnoses. Affected patients often undergo imaging during their evaluation, and a radiologist familiar with the specific and often subtle imaging patterns of these infections can add important clinical value. The authors review the multimodality thoracic, abdominal, and musculoskeletal imaging findings of zoonotic bacterial (eg, Bartonella henselae, Pasteurella multocida, Francisella tularensis, Coxiella burnetii, and Brucella species), spirochetal (eg, Leptospira species), and parasitic (eg, Echinococcus, Paragonimus, Toxocara, and Dirofilaria species) infections that are among the more commonly encountered zoonoses in the United States. Relevant clinical, epidemiologic, and pathophysiologic clues such as exposure history, occupational risk factors, and organism life cycles are also reviewed. Although many of the imaging findings of zoonotic infections overlap with those of nonzoonotic infections, granulomatous diseases, and malignancies, radiologists' familiarity with the imaging patterns can aid in the differential diagnosis in a patient with a suspected or unsuspected zoonotic infection. © RSNA, 2023 Quiz questions for this article are available through the Online Learning Center.

Diagnostic and Imaging Approaches to Chest Wall Lesions.

Chest wall lesions are relatively uncommon and may be challenging once they are encountered on images. Radiologists may detect these lesions incidentally at examinations performed for other indications, or they may be asked specifically to evaluate a suspicious lesion. While many chest wall lesions have characteristic imaging findings that can result in an accurate diagnosis with use of imaging alone, other entities are difficult to distinguish at imaging because there is significant overlap among them. The interpreting radiologist should be familiar with the imaging features of both "do not touch" benign entities (which can be confidently diagnosed with imaging only, with no need for biopsy or resection unless the patient is symptomatic) and lesions that cannot be confidently characterized and thus require further workup. CT and MRI are the main imaging modalities used to assess the chest wall, with each having different benefits and drawbacks. Chest wall lesions can be classified according to their predominant composition: fat, calcification and ossification, soft tissue, or fluid. The identification or predominance of signal intensities or attenuation for these findings, along with the patient age, clinical history, and lesion location, can help establish the appropriate differential diagnosis. In addition, imaging findings in other organs, such as the lungs or upper abdomen, can at times provide clues to the underlying diagnosis. The authors review different chest wall lesions classified on the basis of their composition and highlight the imaging findings that can assist the radiologist in narrowing the differential diagnosis and guiding management. ©RSNA, 2022.

Epidemiology and Survival of Colorectal Cancer in Lebanon: A Sub-National Retrospective Analysis.

BACKGROUND: Scarce data exist about colorectal cancer (CRC) presentation and outcomes in Lebanon. The aim of this study is to describe the characteristics of Lebanese patients diagnosed with colorectal cancer, particularly the method of detection, age of onset, stage at presentation, treatment modalities, and survival. METHODS: This is a retrospective study of a cohort of patients with CRC, diagnosed between 2005 and 2010, admitted to 6 major university-affiliated medical centers in Lebanon. RESULTS: The total sample consisted of 586 patients (median age: 64 years; M:F ratio: 1.25). The most common presenting symptoms were changes in bowel habits, abdominal pain, and blood per rectum. Only 3% had been diagnosed by screening colonoscopy. Of the patients diagnosed with CRC younger than 50 years of age, 72.5% had a positive family history (P = .07). More than two-thirds of patients had an advanced stage of the disease III and IV at presentation. The Kaplan-Meier-estimated survival rate was 0%, 44.5%, 70.2%, and 78.5% for those with stage IV, III, II, and I, respectively (P = .0001), and did not vary by age nor gender of the patient. There was no differential in survival estimate for patients with stage II and III by number of chemotherapy cycles received. However, there was a significant difference in median survivorship for patients with metastatic stage IV disease; those who received less than or equal to 9 cycles had a median survivorship of 2 years (CI: 1.31-2.68) compared to 4 years (CI: 2.36-5.63) for those who received more than 9 cycles (P = .047). The cox regression showed while controlling for age and gender that patients diagnosed at stage IV had a hazard ratio of 8.81 (3.20-24.22) compared to those who were diagnosed at stage I (P = .047). CONCLUSIONS: Lebanese patients affected by colorectal cancer tend to present with advanced disease stages, leading to poor prognosis and survival.

Acute myocarditis after a second dose of the mRNA COVID-19 vaccine: a report of two cases.

We report two cases of myocarditis, in two young and previously healthy individuals, temporally related to the second dose of the mRNA-COVID-19 vaccine. Both patients developed acute chest pain, changes on electrocardiogram (ECG), and elevated serum troponin within two days of receiving their second dose. Cardiac magnetic resonance (CMR) findings were consistent with acute myocarditis.

Abdominal Imaging Manifestations of Recreational Drug Use.

Recreational drug use is a burgeoning health issue worldwide, with a variety of presenting symptoms and complications. These complications can be secondary to the toxic effects of the drug itself, drug impurities, and nonsterile injection. The abdominal radiologist is likely to encounter patients who use drugs recreationally and may be responsible for recognizing and reporting these acute conditions, which in some cases can be life threatening. Because these patients often present with an altered mental state and may deny or withhold information on drug use, the underlying cause may be difficult to determine. The most commonly used drugs worldwide include cocaine, cannabinoids, opioids, and amphetamines and their derivatives. Complications of use of these drugs that can be seen at abdominopelvic CT can involve multiple organ systems, including the soft tissue and gastrointestinal, genitourinary, vascular, and musculoskeletal systems. A diverse range of abdominal complications associated with these drugs can be seen at imaging, including disseminated infections, gastrointestinal ischemia, and visceral infarction. Radiologists should be familiar with the imaging findings of these complications to accurately diagnose these entities and help guide workup and patient treatment. ©RSNA, 2020.

Mechanism of Human Fetal Membrane Biomechanical Weakening, Rupture and Potential Targets for Therapeutic Intervention.

Using a novel in vitro model system combining biochemical/histologic with bioengineering approaches has provided significant insights into the physiology of fetal membrane weakening and rupture along with potential mechanistic reasons for lack of efficacy of currently clinically used agents to prevent preterm premature rupture of the membranes (pPROM) and preterm births. Likewise, the model has also facilitated screening of agents with potential for preventing pPROM and preterm birth.

The nonlinear relationship between speed of sound and compression in articular cartilage: Measurements and modeling.

We measured speed of sound in bovine articular cartilage as a function of compressive strain. Using techniques we developed, it was possible to apply strain starting from the unstrained, full height of a sample. Our measurements showed that speed of sound was not a monotonic function of strain as reported in earlier investigations. Speed increased with increasing strain over a range of lower strains. It reached a maximum, and then decreased as the strain increased further. These results were corroborated using a model of wave propagation in deformable porous materials. Using this model, we also established conditions under which a maximum in the speed would exist for samples in compression. Our measurements and analysis resolve the conflicting results reported in previous studies.

Apparatus and Method for Rapid Detection of Acoustic Anisotropy in Cartilage.

PURPOSE: Articular cartilage is known to be mechanically anisotropic. In this paper, the acoustic anisotropy of bovine articular cartilage and the effects of freeze-thaw cycling on acoustic anisotropy were investigated. METHODS: We developed apparatus and methods that use a magnetic L-shaped sample holder, which allowed minimal handling of a tissue, reduced the number of measurements compared to previous studies, and produced highly reproducible results. RESULTS: SOS was greater in the direction perpendicular to the articular surface compared to the direction parallel to the articular surface (N=17, P = 0.00001). Average SOS was 1,758 ± 107 m/s perpendicular to the surface, and 1,617 ± 55 m/s parallel to it. The average percentage difference in SOS between the perpendicular and parallel directions was 8.2% (95% CI: 5.4% to 11%). Freeze-thaw cycling did not have a significant effect on SOS (P>0.4). CONCLUSION: Acoustic measurement of tissue properties is particularly attractive for work in our laboratory since it has the potential for nondestructive characterization of the properties of developing engineered cartilage. Our approach allowed us to observe acoustic anisotropy of articular cartilage rapidly and reproducibly. This property was not significantly affected by freeze-thawing of the tissue samples, making cryopreservation practical for these assays.

A Review of Viral-Related Malignancies and the Associated Imaging Findings.

OBJECTIVE. Imaging plays an important role in the diagnosis and staging of malignancies. Many common lymphoproliferative and other solid tumor malignancies can be viral-related. CONCLUSION. This review discusses the imaging findings that can be associated with common viral-induced malignancies. Knowledge of these imaging presentations can help narrow the differential diagnosis to reach a specific diagnosis through a precise workup and proper management.

Granulocyte macrophage colony stimulating factor (GM-CSF), the critical intermediate of inflammation-induced fetal membrane weakening, primarily exerts its weakening effect on the choriodecidua rather than the amnion.

INTRODUCTION: We have previously demonstrated two associations of PPROM, (1) inflammation/infection (modeled by tumor necrosis factor (TNF)) and (2) decidual bleeding (modeled by thrombin), both decrease fetal membrane (FM) rupture strength in-vitro. Furthermore, Granulocyte-Macrophage-Colony-Stimulating-Factor (GM-CSF) induced by both TNF and thrombin is a critical intermediate, necessary and sufficient for weakening by either agent. The amnion is the strength component of FM and must weaken for FM to rupture. It is unclear whether GM-CSF weakens amnion (AM) directly, or initially targets choriodecidua (CD) which secondarily releases agents to act on amnion. METHODS: Full thickness FM fragments were treated with/without GM-CSF. Some were preincubated with alpha-lipoic acid (LA), a known inhibitor of FM weakening. The FM fragments were then strength-tested. Separately, FM fragments were initially separated to AM and CD. AM fragments were cultured with Medium ± GM-CSF and then strength-tested. In other experiments, CD fragments were cultured with Medium, GM-CSF, LA, or LA + GM-CSF. Conditioned medium from each group was then incubated with AM. AM was then strength-tested. Matrix Metalloproteinases (MMPs) and Tissue Inhibitors of Matrix Metalloproteinases (TIMPs) were analyzed by Mutiplex Elisa. RESULTS: GM-CSF weakened intact FM which was blocked by LA. GM-CSF did not weaken isolated AM. However, GM-CSF conditioned CD media weakened AM and this weakening was inhibited by LA. GM-CSF treatment of CD increased MMPs 2, 9, and 10, and decreased TIMPs 1-3. LA reversed these effects. CONCLUSIONS: GM-CSF does not weaken amnion directly; GM-CSF acts on CD to increase proteases and decrease anti-proteases which secondarily weaken the amnion.

Rapid Detection of Shear-Induced Damage in Tissue-Engineered Cartilage Using Ultrasound.

Previous investigations have shown that tissue-engineered articular cartilage can be damaged under a combination of compression and sliding shear. In these cases, damage was identified in histological sections after a test was completed. This approach is limited, in that it does not identify when damage occurred. This especially limits the utility of an assay for evaluating damage when comparing modifications to a tissue-engineering protocol. In this investigation, the feasibility of using ultrasound (US) to detect damage as it occurs was investigated. US signals were acquired before, during, and after sliding shear, as were stereomicroscope images of the cartilage surface. Histology was used as the standard for showing if a sample was damaged. We showed that US reflections from the surface of the cartilage were attenuated due to roughening following sliding shear. Furthermore, it was shown that by scanning the transducer across a sample, surface roughness and erosion following sliding shear could be identified. Internal delamination could be identified by the appearance of new echoes between those from the front and back of the sample. Thus, it is feasible to detect damage in engineered cartilage using US.

In an in-vitro model using human fetal membranes, α-lipoic acid inhibits inflammation induced fetal membrane weakening.

INTRODUCTION: We established an in-vitro model for the study of human fetal membrane (FM) weakening leading to pPROM. In this model, granulocyte-macrophage colony-stimulating factor (GM-CSF) is a critical intermediate for both tumor necrosis factor-α (TNF; modeling infection/inflammation) and thrombin (modeling decidual bleeding/abruption)-induced weakening. Thus, inhibitors of FM weakening can be categorized as targeting GM-CSF production, GM-CSF downstream action, or both. Most progestogens inhibit both, except 17-α hydroxyprogesterone caproate which inhibits FM weakening at only one point, GM-CSF production. α-lipoic acid (LA), an over-the-counter dietary supplement, has also been previously shown to inhibit TNF and thrombin induced FM weakening. OBJECTIVE: To determine the point of action of LA inhibition of FM weakening. METHODS: FM fragments were mounted in Transwell inserts and preincubated with/without LA/24 h, then with/without addition of TNF, thrombin or GM-CSF. After 48 h, medium was assayed for GM-CSF, and FM fragments were rupture-strength tested. RESULTS: TNF and thrombin both weakened FM and increased GM-CSF levels. GM-CSF also weakened FM. LA inhibited both TNF and thrombin induced FM weakening and concomitantly inhibited the increase in GM-CSF in a concentration-dependent manner. In addition, LA inhibited GM-CSF induced FM weakening in a concentration dependent manner. CONCLUSIONS: LA blocks TNF and thrombin induced FM weakening at two points, inhibiting both GM-CSF production and downstream action. Thus, we speculate that LA may be a potential standalone therapeutic agent, or supplement to current therapy for prevention of pPROM related spontaneous preterm birth, if preclinical studies to examine feasibility and safety during pregnancy are successfully accomplished.

From Bouveret's Syndrome to Gallstone Ileus: The Journey of a Migrating Stone!

Bouveret's syndrome, first described in 1896, is an unusual cause of gastric outlet obstruction secondary to large gallstone impaction in the proximal duodenum after migration through a cholecystoduodenal fistula. Stone migration has been previously described after endoscopic or surgical fragmentation. However, this is the first reported case, in our knowledge, where the stone migrated after oral contrast administration a few days after the onset of symptoms, causing a distal gallstone ileus.

Thyroxine Increases Collagen Type II Expression and Accumulation in Scaffold-Free Tissue-Engineered Articular Cartilage.

Low collagen accumulation in the extracellular matrix is a pressing problem in cartilage tissue engineering, leading to a low collagen-to-glycosaminoglycan (GAG) ratio and poor mechanical properties in neocartilage. Soluble factors have been shown to increase collagen content, but may result in a more pronounced increase in GAG content. Thyroid hormones have been reported to stimulate collagen and GAG production, but reported outcomes, including which specific collagen types are affected, are variable throughout the literature. Here we investigated the ability of thyroxine (T4) to preferentially stimulate collagen production, as compared with GAG, in articular chondrocyte-derived scaffold-free engineered cartilage. Dose response curves for T4 in pellet cultures showed that 25 ng/mL T4 increased the total collagen content without increasing the GAG content, resulting in a statistically significant increase in the collagen-to-GAG ratio, a fold change of 2.3 ± 1.2, p < 0.05. In contrast, another growth factor, TGFß1, increased the GAG content in excess of threefold more than the increase in collagen. In large scaffold-free neocartilage, T4 also increased the total collagen/DNA at 1 month and at 2 months (fold increases of 2.1 ± 0.8, p < 0.01 and 2.1 ± 0.4, p < 0.001, respectively). Increases in GAG content were not statistically significant. The effect on collagen was largely specific to collagen type II, which showed a 2.8 ± 1.6-fold increase of COL2A1 mRNA expression (p < 0.01). Western blots confirmed a statistically significant increase in type II collagen protein at 1 month (fold increase of 2.2 ± 1.8); at 2 months, the fold increase of 3.7 ± 3.3 approached significance (p = 0.059). Collagen type X protein was less than the 0.1 µg limit of detection. T4 did not affect COL10A1 and COL1A2 gene expression in a statistically significant manner. Biglycan mRNA expression increased 2.6 ± 1.6-fold, p < 0.05. Results of this study show that an optimized dosage of T4 is able to increase collagen type II content, and do so preferential to GAG. Moreover, the upregulation of COL2A1 gene expression and type II collagen protein accumulation, without a concomitant increase in collagens type I or type X, signifies a direct enhancement of chondrogenesis of hyaline articular cartilage without the induction of terminal differentiation.

In an in-vitro model using human fetal membranes, 17-α hydroxyprogesterone caproate is not an optimal progestogen for inhibition of fetal membrane weakening.

BACKGROUND: The progestogen 17-α hydroxyprogesterone caproate (17-OHPC) is 1 of only 2 agents recommended for clinical use in the prevention of spontaneous preterm delivery, and studies of its efficacy have been conflicting. We have developed an in-vitro model to study the fetal membrane weakening process that leads to rupture in preterm premature rupture of the fetal membranes (pPROM). Inflammation/infection associated with tumor necrosis factor-α (TNF-α) induction and decidual bleeding/abruption associated thrombin release are leading causes of preterm premature rupture of the fetal membranes. Both agents (TNF-α and thrombin) cause fetal membrane weakening in the model system. Furthermore, granulocyte-macrophage colony-stimulating factor (GM-CSF) is a critical intermediate for both TNF-α and thrombin-induced fetal membrane weakening. In a previous report, we demonstrated that 3 progestogens, progesterone, 17-alpha hydroxyprogesterone (17-OHP), and medroxyprogesterone acetate (MPA), each inhibit both TNF-α- and thrombin-induced fetal membrane weakening at 2 distinct points of the fetal membrane weakening pathway. Each block both the production of and the downstream action of the critical intermediate granulocyte-macrophage colony-stimulating factor. OBJECTIVE: The objective of the study was to characterize the inhibitory effects of 17-OHPC on TNF-α- and thrombin-induced fetal membrane weakening in vitro. STUDY DESIGN: Full-thickness human fetal membrane fragments from uncomplicated term repeat cesarean deliveries were mounted in 2.5 cm Transwell inserts and cultured with/without 17-alpha hydroxyprogesterone caproate (10-9 to 10-7 M). After 24 hours, medium (supernatant) was removed and replaced with/without the addition of tumor necrosis factor-alpha (20 ng/mL) or thrombin (10 U/mL) or granulocyte-macrophage colony-stimulating factor (200 ng/mL). After 48 hours of culture, medium from the maternal side compartment of the model was assayed for granulocyte-macrophage colony-stimulating factor and the fetal membrane fragments were rupture strength tested. RESULTS: Tumor necrosis factor-alpha and thrombin both weakened fetal membranes (43% and 62%, respectively) and increased granulocyte-macrophage colony-stimulating factor levels (3.7- and 5.9-fold, respectively). Pretreatment with 17-alpha hydroxyprogesterone caproate inhibited both tumor necrosis factor-alpha- and thrombin-induced fetal membrane weakening and concomitantly inhibited the induced increase in granulocyte-macrophage colony-stimulating factor in a concentration-dependent manner. However, contrary to our prior reports regarding progesterone and other progestogens, 17-alpha hydroxyprogesterone caproate did not also inhibit granulocyte-macrophage colony-stimulating factor-induced fetal membrane weakening. CONCLUSION: 17-Alpha hydroxyprogesterone caproate blocks tumor necrosis factor-alpha- and thrombin-induced fetal membrane weakening by inhibiting the production of granulocyte-macrophage colony-stimulating factor. However, 17-alpha hydroxyprogesterone caproate did not also inhibit granulocyte-macrophage colony-stimulating factor-induced weakening. We speculate that progestogens other than 17-alpha hydroxyprogesterone caproate may be more efficacious in preventing preterm premature rupture of the fetal membranes-related spontaneous preterm birth.

Micrometer scale guidance of mesenchymal stem cells to form structurally oriented large-scale tissue engineered cartilage.

Current clinical methods to treat articular cartilage lesions provide temporary relief of the symptoms but fail to permanently restore the damaged tissue. Tissue engineering, using mesenchymal stem cells (MSCs) combined with scaffolds and bioactive factors, is viewed as a promising method for repairing cartilage injuries. However, current tissue engineered constructs display inferior mechanical properties compared to native articular cartilage, which could be attributed to the lack of structural organization of the extracellular matrix (ECM) of these engineered constructs in comparison to the highly oriented structure of articular cartilage ECM. We previously showed that we can guide MSCs undergoing chondrogenesis to align using microscale guidance channels on the surface of a two-dimensional (2-D) collagen scaffold, which resulted in the deposition of aligned ECM within the channels and enhanced mechanical properties of the constructs. In this study, we developed a technique to roll 2-D collagen scaffolds containing MSCs within guidance channels in order to produce a large-scale, three-dimensional (3-D) tissue engineered cartilage constructs with enhanced mechanical properties compared to current constructs. After rolling the MSC-scaffold constructs into a 3-D cylindrical structure, the constructs were cultured for 21days under chondrogenic culture conditions. The microstructure architecture and mechanical properties of the constructs were evaluated using imaging and compressive testing. Histology and immunohistochemistry of the constructs showed extensive glycosaminoglycan (GAG) and collagen type II deposition. Second harmonic generation imaging and Picrosirius red staining indicated alignment of neo-collagen fibers within the guidance channels of the constructs. Mechanical testing indicated that constructs containing the guidance channels displayed enhanced compressive properties compared to control constructs without these channels. In conclusion, using a novel roll-up method, we have developed large scale MSC based tissue-engineered cartilage that shows microscale structural organization and enhanced compressive properties compared to current tissue engineered constructs. STATEMENT OF SIGNIFICANCE: Tissue engineered cartilage constructs made with human mesenchymal stem cells (hMSCs), scaffolds and bioactive factors are a promising solution to treat cartilage defects. A major disadvantage of these constructs is their inferior mechanical properties compared to the native tissue, which is likely due to the lack of structural organization of the extracellular matrix of the engineered constructs. In this study, we developed three-dimensional (3-D) cartilage constructs from rectangular scaffold sheets containing hMSCs in micro-guidance channels and characterized their mechanical properties and metabolic requirements. The work led to a novel roll-up method to embed 2-D microscale structures in 3-D constructs. Further, micro-guidance channels incorporated within the 3-D cartilage constructs led to the production of aligned cell-produced matrix and enhanced mechanical function.

Scaffold-free cartilage subjected to frictional shear stress demonstrates damage by cracking and surface peeling.

Scaffold-free engineered cartilage is being explored as a treatment for osteoarthritis. In this study, frictional shear stress was applied to determine the friction and damage behaviour of scaffold-free engineered cartilage, and tissue composition was investigated as it related to damage. Scaffold-free engineered cartilage frictional shear stress was found to exhibit a time-varying response similar to that of native cartilage. However, damage occurred that was not seen in native cartilage, manifesting primarily as tearing through the central plane of the constructs. In engineered cartilage, cells occupied a significantly larger portion of the tissue in the central region where damage was most prominent (18 ± 3% of tissue was comprised of cells in the central region vs 5 ± 1% in the peripheral region; p < 0.0001). In native cartilage, cells comprised 1-4% of tissue for all regions. Average bulk cellularity of engineered cartilage was also greater (68 × 103 ± 4 × 103 vs 52 × 103 ± 22 × 103 cells/mg), although this difference was not significant. Bulk tissue comparisons showed significant differences between engineered and native cartilage in hydroxyproline content (8 ± 2 vs 45 ± 3 µg HYP/mg dry weight), solid content (12.5 ± 0.4% vs 17.9 ± 1.2%), shear modulus (0.06 ± 0.02 vs 0.15 ± 0.07 MPa) and aggregate modulus (0.12 ± 0.03 vs 0.32 ± 0.14 MPa), respectively. These data indicate that enhanced collagen content and more uniform extracellular matrix distribution are necessary to reduce damage susceptibility. Copyright © 2014 John Wiley & Sons, Ltd.

Malignancy after Solid Organ Transplantation: Comprehensive Imaging Review.

Life expectancies for solid organ recipients as well as graft survival rates for these patients have improved over the years because of advanced immunosuppressive therapies; however, with chronic use of these drugs, posttransplant malignancy has become one of the leading causes of morbidity for them. The risk of carcinogenesis in transplant recipients is significantly higher than for the general population and cancers tend to manifest at an advanced stage. Posttransplant malignancies are thought to develop by three mechanisms: de novo development, donor-related transmission, and recurrence of a recipient's pretransplant malignancy. Although nonmelanoma skin cancer, Kaposi sarcoma, posttransplant lymphoproliferative disorder, anogenital cancer, and lung cancer are malignancies that are thought to arise de novo, malignant melanoma and cancers that arise in the renal allograft are frequently donor related. Hepatocellular carcinomas and cholangiocarcinomas have a greater tendency to recur in liver transplant recipients. An altered or deranged immune system caused by chronic immunosuppression is considered to be one of the major contributing factors to carcinogenesis. The proposed pathogenic mechanisms for oncogenesis include impaired immunosurveillance of neoplastic cells, weakened immune activity against oncogenic viruses, and direct carcinogenic effects of immunosuppressive agents. Imaging plays an important role in screening, follow-up, and long-term surveillance in patients with malignancies because key imaging features can guide in their timely diagnosis. However, some benign entities such as transplant-related renal fibrosis, biliary necrosis, and infectious nodules in the lungs mimic malignancies and require pathologic confirmation. Management strategies that can improve malignancy-related morbidity and mortality in transplant recipients include prevention of risk factors, appropriate modulation of immunosuppressive agents, prophylaxis against infection-related malignancies, and use of intensive targeted screening programs. (©)RSNA, 2016.