Herein we report a new design for acoustic nanoswimmers, making use of a nanoshell geometry that was synthesized using a sphere template process. Such shell-shaped nanomotors display highly efficient acoustic propulsion on the nanoscale by converting energy from the ambient acoustic field into motion. The propulsion mechanism of the nanoshell motors relies on acoustic streaming stress over the asymmetric surface to produce the driving force for motion. The shell-shaped nanomotors offer a high surface area to volume ratio, allow for efficient scalability and provide higher cargo towing capacity (in comparison to acoustically propelled nanowires). Furthermore, a detailed study of the parameters relevant to propulsion performance, including the material density, size and shape of the motors, reveals that the nanoshell motors exhibit a different propulsion behavior from that predicted by recent theoretical and experimental models for acoustically propelled nanomotors. Such findings indicate that further studies are needed to predict the behavior of acoustic nanomotors with different geometry designs. Practical applications of the new nanoshell motors, including "on-the-move" capture and the transport of multiple cargoes and internalization and movement inside live MCF-7 cancer cells, are demonstrated. These capabilities hold considerable promise for designing fuel-free nanoswimmers capable of performing complex tasks for diverse biomedical applications.

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Objective Arterial calcification due to deficiency of CD73 (ACDC) is a hereditary autosomal recessive ectopic mineralization syndrome caused by loss-of-function mutations in the 5'-nucleotidase Ecto (NT5E) gene. Periarticular calcification has been reported but the clinical characterization of arthritis as well as the microstructure and chemical composition of periarticular calcifications and synovial fluid crystals has not been systematically investigated. Methods Eight ACDC patients underwent extensive rheumatological and radiological evaluation over a period of 11 years. Periarticular and synovial biopsies were obtained from four patients. Characterization of crystal composition was evaluated by compensated polarized light microscopy, Alizarin red staining for synovial fluid along with x-ray diffraction and x-ray micro tomosynthesis for periarticular calcification. Results Arthritis in ACDC patients has a clinical presentation of mixed erosive-degenerative joint changes with a median onset of articular symptoms at 17 years of age and progresses over time to the development of fixed deformities and functional limitations of small peripheral joints with eventually, larger joint and distinct axial involvement later in life. We have identified calcium pyrophosphate (CPP) and calcium hydroxyapatite (CHA) crystals in synovial fluid specimens and determined that CHA crystals are the principal component of periarticular calcifications. Conclusion This is the largest study in ACDC patients to describe erosive peripheral arthropathy and axial enthesopathic calcifications over a period of 11 years and the first to identify the composition of periarticular calcifications and synovial fluid crystals. ACDC should be considered among the genetic causes of early-onset osteoarthritis, as musculoskeletal disease signs may often precede vascular symptoms.

A 54-year old female patient with the genetic disease of arterial calcification due to deficiency of CD73 was studied under the Undiagnosed Disease Program of the National Institutes of Health. She presented with symptoms of claudication in her 40s and later developed arthritic symptoms, ectopic calcification in her left hand and severe arterial calcifications of the lower extremities. Since little was known about the composition of the calcifications in arterial calcification due to deficiency of CD73, we investigated their chemical identity and microscopic morphology in this patient with imaging and x-ray diffraction analysis. We found that, microscopically, the bulk calcifications consisted of fragments of either solid or porous internal structure. Both periarticular and arterial calcifications were primarily hydroxyapatite crystals of the same crystalline anisotropy, but different crystalline grain sizes. This was consistent with the presence of hydroxyapatite crystals along with birefringent calcium pyrophosphate dihydrate crystals in the synovial fluid of the patients by polarized light microscopy. The result suggests that tissue calcification in both locations follow a similar biochemical mechanism caused by an increase in extracellular tissue-nonspecific alkaline phosphatase activity.