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Purpose: To describe a digital fabrication method used for custom MRI receive coils with vacuum forming and electroless copper plating., Methods: Our process produces intricate copper traces on curved surfaces. A three-dimensional scan of a desired anatomy is obtained and used to design coil elements. The layout is predistorted with a self built simulation of the vacuum forming process and the geometric overlaps are tested with electromagnetic simulation software. The desired coil geometry is patterned onto a polycarbonate sheet by sandblasting through a tape mask. The sandblasted areas are then catalyzed with a palladium-tin solution and vacuum formed. The catalyzed, three-dimensional part is placed into a custom built plating tank and copper plated. Electronic components are attached to the copper traces to form resonant receive coils. The methods described here are demonstrated and tested with an 8 channel visual cortex coil array., Results: The prototype coils exhibit quality factor ratios higher than three, indicating body noise dominance. The coil array shows high signal-to-noise ratio (SNR) near the periphery of a head shaped phantom. In vivo images with up to 0 . 37 × 0 . 37 × 0 . 67   mm 3 $$ 0.37\times 0.37\times 0.67\;{\mathrm{mm}}^3 $$ spatial resolution were acquired on a human volunteer., Conclusion: This work presents the first example of vacuum formed coils with direct electroless copper plating. Our fabrication method results in coil arrays that are in close proximity to the body. This methods described here may enable the rapid development of a set of coils of different sizes for applications including longitudinal fMRI studies and MR-guided therapies., (© 2022 International Society for Magnetic Resonance in Medicine.)

Background: Genomic testing is increasingly performed in oncology, but concerns remain regarding the clinician's ability to interpret results. In the current study, the authors sought to determine the agreement between physicians and genomic annotators from the Precision Oncology Decision Support (PODS) team at The University of Texas MD Anderson Cancer Center in Houston regarding actionability and the clinical use of test results., Methods: On a prospective protocol, patients underwent clinical genomic testing for hotspot mutations in 46 or 50 genes. Six months after sequencing, physicians received questionnaires for patients who demonstrated a variant in an actionable gene, investigating their perceptions regarding the actionability of alterations and clinical use of these findings. Genomic annotators independently classified these variants as actionable, potentially actionable, unknown, or not actionable., Results: Physicians completed 250 of 288 questionnaires (87% response rate). Physicians considered 168 of 250 patients (67%) as having an actionable alteration; of these, 165 patients (98%) were considered to have an actionable alteration by the PODS team and 3 were of unknown significance. Physicians were aware of genotype-matched therapy available for 119 patients (71%) and 48 of these 119 patients (40%) received matched therapy. Approximately 46% of patients in whom physicians regarded alterations as not actionable (36 of 79 patients) were classified as having an actionable/potentially actionable mutation by the PODS team. However, many of these were only theoretically actionable due to limited trials and/or therapies (eg, KRAS)., Conclusions: Physicians are aware of recurrent mutations in actionable genes on "hotspot" panels. As larger genomic panels are used, there may be a growing need for annotation of actionability. Decision support to increase awareness of genomically relevant trials and novel treatment options for recurrent mutations (eg, KRAS) also are needed. Cancer 2018;124:966-72. © 2017 American Cancer Society., (© 2017 American Cancer Society.)

Two unique cases of rheumatoid nodules affecting the larynx are reported. These subcutaneous nodules represent localized laryngeal involvement from autoimmune disorders. The otolaryngologist should be aware of these possibilities as part of the differential diagnosis in the workup of dysphonia.

Antibodies directed against the epidermal growth factor receptor may impede proliferation and induce differentiation of head and neck squamous cell carcinoma. To test this hypothesis, we examined the effect of monoclonal antibody 528 directed against epidermal growth factor receptor on the proliferation and differentiation of monolayer cells and multicenter tumor spheroids from three head and neck squamous cell carcinoma cell lines (1483, MDA 686Ln, and MDA 886Ln) and the epidermal growth factor-responsive vulvar carcinoma A431. All head and neck squamous cell carcinoma lines were shown to express high levels of epidermal growth factor receptor by Scatchard analyses. Epidermal growth factor inhibited the growth of monolayer cells but stimulated the growth of 886 and A431 multicellular tumor spheroids. Epidermal growth factor modulated the differentiation of A431 and 686 with respect to involucrin immunohistochemistry and cornified enveloped competency. Monoclonal antibody 528 directed against epidermal growth factor receptor inhibited cellular proliferation as measured by cell number, thymidine incorporation, and multicellular tumor spheroid volume. A mild promotion of differentiation was observed in the epidermal growth factor-responsive cells. In conclusion, monoclonal antibody 528 directed against epidermal growth factor receptor inhibits growth of head and neck squamous cell carcinoma cells bearing high levels of epidermal growth factor receptors and promotes differentiation in some tumors. The use of a multicellular tumor spheroid model to evaluate growth factor responsiveness and inhibition of proliferation may more accurately reflect in vivo tumor growth than monolayer cells. Antibodies against epidermal growth factor receptor may prove effective in modulating disease progression in patients with head and neck squamous cell carcinoma.

Twenty-nine patients with extensive disease, small-cell carcinoma of the lung, were treated with two cycles of intensive combination chemotherapy: HexaVAC (hexamethylmelamine, vincristine, Adriamycin, cyclophosphamide). Responders received prophylactic cranial radiation (2000 rad/10 fractions) and non cross resistant chemotherapy via a schedule of alternating cycles of CMV (cyclophosphamide, methotrexate, VP-16-213) and AMV (Adriamycin, methotrexate, VP-16-213). Whenever a complete response was achieved, consolidation radiotherapy was given to the lung primary (4000 rad/20 fractions, split dose) and abdominal metastases (2000 rad/10 fractions) synchronous with CMV therapy. The complete response rate was 14% with HexaVAC, but increased to 38% during CMV/AMV. Total response rate (complete and partial) was 59% and median survival was 42 weeks. Prophylactic brain radiation prevented clinical relapse in the brain in all 14 patients who received it. However, consolidation radiotherapy failed to prevent clinical relapse in the lung and/or liver, and therapeutic brain radiation (3000 rad) failed to prevent relapse in that site. The simultaneous administration of radiotherapy and chemotherapy was well-tolerated although two patients with poor performance status died of infectious complications while leukopenic. In spite of the high response rate, durable remissions with prolonged disease free survival were rare. Further evaluation of induction, consolidation, and maintenance modes of therapy are indicated.