Compressed sensing with signal averaging for improved sensitivity and motion artifact reduction in fluorine‐19 MRI

Fluorine‐19 (¹⁹F) MRI of injected perfluorocarbon emulsions (PFCs) allows for the non‐invasive quantification of inflammation and cell tracking, but suffers from a low signal‐to‐noise ratio and extended scan time. To address this limitation, we tested the hypotheses that a ¹⁹F MRI pulse sequence that combines a specific undersampling regime with signal averaging has both increased sensitivity and robustness against motion artifacts compared with a non‐averaged fully sampled pulse sequence, when both datasets are reconstructed with compressed sensing. As a proof of principle, numerical simulations and phantom experiments were performed on selected variable ranges to characterize the point spread function of undersampling patterns, as well as the vulnerability to noise of undersampling and reconstruction parameters with paired numbers of x signal averages and acceleration factor x (NAx ‐AFx ). The numerical simulations demonstrated that a probability density function that uses 25% of the samples to fully sample the k‐space central area allowed for an optimal balance between limited blurring and artifact incoherence. At all investigated noise levels, the Dice similarity coefficient (DSC) strongly depended on the regularization parameters and acceleration factor. In phantoms, the motion robustness of an NA8‐AF8 undersampling pattern versus NA1‐AF1 was evaluated with simulated and real motion patterns. Differences were assessed with the DSC, which was consistently higher for the NA8‐AF8 compared with the NA1‐AF1 strategy, for both simulated and real cyclic motion patterns (P < 0.001). Both strategies were validated in vivo in mice (n = 2) injected with perfluoropolyether. Here, the images displayed a sharper delineation of the liver with the NA8‐AF8 strategy than with the NA1‐AF1 strategy. In conclusion, we validated the hypotheses that in ¹⁹F MRI the combination of undersampling and averaging improves both the sensitivity and the robustness against motion artifacts.     

Nerve Transfers for Treatment of Isolated Axillary Nerve Injuries

BACKGROUND:

The most common neurological defect in traumatic anterior glenohumeral dislocation is isolated axillary nerve palsy. Most recover spontaneously; however, some have persistent axillary neuropathy. An intact rotator cuff may compensate for an isolated axillary nerve injury; however, given the high rate of rotator cuff pathology with advancing age, patients with an axillary nerve injury are at risk for complete shoulder disability.

OBJECTIVE:

To review reconstruction of the axillary nerve to alleviate shoulder pain, augment shoulder stability, abduction and external rotation to alleviate sole reliance on the rotator cuff to move and stabilize the shoulder.

METHODS:

A retrospective review of 10 patients with an isolated axillary nerve injury and an intact rotator cuff who underwent a triceps nerve branch to axillary nerve transfer was performed. Patient demographics, surgical technique, deltoid strength, donor-site morbidity, complications and time to surgery were evaluated.

RESULTS:

Ten male patients, mean age 38.3 years (range 18 to 66 years), underwent a triceps to axillary nerve transfer for isolated axillary nerve injury 7.4 months (range five to 12 months) post-traumatic shoulder dislocation. Deltoid function was British Medical Research Council grade 0/5 in all patients preoperatively and ≥3/5 deltoid strength in eight patients at final follow-up (14.8 months [range 12 to 25 months]). There were no complications and no donor-site morbidity.

CONCLUSION:

A triceps to axillary nerve transfer for isolated axillary neuropathy following traumatic shoulder dislocation improved shoulder pain, stability and deltoid strength, and potentially preserves shoulder function with advancing age by alleviating sole reliance on the rotator cuff for shoulder abduction and external rotation.     

Off-resonance magnetic resonance angiography improves visualization of in-stent lumen in peripheral nitinol stents compared to conventional T1-weighted acquisitions: an in vitro comparison study

To compare the value of inversion recovery with on-resonant water suppression (IRON) to conventional T1-weighted (T1w) MRA and computed tomography angiography (CTA) for visualization of peripheral nitinol stents. We visualized 14 different peripheral nitinol stents in vitro both using Gadolinium (Gd) and ultrasmall superparamagnetic iron nanoparticles (USPIOs) for conventional T1w and IRON-MRA using clinical grade 1.5T MR scanner and iodinated contrast material for CTA using a 256-slice CT scanner. Parameter assessment included signal- and contrast-to-noise ratio (S/CNR), relative in-stent signal and artificial lumen narrowing. X-ray angiography served as gold standard for diameter assessment. Gd-enhanced IRON-MRA exhibited highest in-stent SNR and CNR values compared to conventional T1w MRA (IRON (Gd/USPIO): SNR?=?30?±?3/21?±?2, CNR?=?23?±?2/14?±?1; T1w: SNR?=?16?±?1/14?±?2, CNR?=?12?±?1/10?±?1, all p?<?0.05). Furthermore, IRON-MRA achieved highest relative in-stent signal both using Gd and USPIO (IRON (Gd/USPIO): 121?±?8?%/103?±?6?%; T1w: 73?±?2?%/66?±?4?%; CTA: 84?±?6?%, all p?<?0.05). However, artificial lumen narrowing appeared similar in all imaging protocols (IRON (Gd/USPIO): 21?±?3?%/21?±?2?%; T1w: 16?±?4?%/17?±?3?%; CTA: 19?±?2?%, all p?=?NS). Finally, IRON-MRA provided improvement of the in-stent lumen visualization with an ‘open-close-open’ design, which revealed a complete in-stent signal loss in T1w MRA. IRON-MRA improves in-stent visualization in vitro compared to conventional T1w MRA and CTA. In light of the in vitro results with Gd-enhanced IRON-MRA, the clinical implementation of such an approach appears promising.     

A skin-selective homing mechanism for human immune surveillance T cells

Effective immune surveillance is essential for maintaining protection and homeostasis of peripheral tissues. However, mechanisms controlling memory T cell migration to peripheral tissues such as the skin are poorly understood. Here, we show that the majority of human T cells in healthy skin express the chemokine receptor CCR8 and respond to its selective ligand I-309/CCL1. These CCR8(+) T cells are absent in small intestine and colon tissue, and are extremely rare in peripheral blood, suggesting healthy skin as their physiological target site. Cutaneous CCR8(+) T cells are preactivated and secrete proinflammatory cytokines such as tumor necrosis factor-alpha and interferon-gamma, but lack markers of cytolytic T cells. Secretion of interleukin (IL)-4, IL-10, and transforming growth factor-beta was low to undetectable, arguing against a strict association of CCR8 expression with either T helper cell 2 or regulatory T cell subsets. Potential precursors of skin surveillance T cells in peripheral blood may correspond to the minor subset of CCR8(+)CD25(-) T cells. Importantly, CCL1 is constitutively expressed at strategic cutaneous locations, including dermal microvessels and epidermal antigen-presenting cells. For the first time, these findings define a chemokine system for homeostatic T cell traffic in normal human skin.     

Neurophysiologic monitoring in neurosurgery

This article focuses on the application of neurophysiologic monitoring in uniquely neurosurgical procedures. Neurophysiologic monitoring provides functional testing and mapping to identify neural structures. Once identified, the functionality of the central and peripheral nervous system areas at risk for neurosurgical injury can be monitored. It discusses the use of motor-evoked potentials, sensory evoked potentials, electromyography and electroencephalography to assess neurologic change.     

IL-33 signaling contributes to the pathogenesis of myeloproliferative neoplasms

Myeloproliferative neoplasms (MPNs) are characterized by the clonal expansion of one or more myeloid cell lineage. In most cases, proliferation of the malignant clone is ascribed to defined genetic alterations. MPNs are also associated with aberrant expression and activity of multiple cytokines; however, the mechanisms by which these cytokines contribute to disease pathogenesis are poorly understood. Here, we reveal a non-redundant role for steady-state IL-33 in supporting dysregulated myelopoiesis in a murine model of MPN. Genetic ablation of the IL-33 signaling pathway was sufficient and necessary to restore normal hematopoiesis and abrogate MPN-like disease in animals lacking the inositol phosphatase SHIP. Stromal cell–derived IL-33 stimulated the secretion of cytokines and growth factors by myeloid and non-hematopoietic cells of the BM, resulting in myeloproliferation in SHIP-deficient animals. Additionally, in the transgenic JAK2^V617F model, the onset of MPN was delayed in animals lacking IL-33 in radio-resistant cells. In human BM, we detected increased numbers of IL-33–expressing cells, specifically in biopsies from MPN patients. Exogenous IL-33 promoted cytokine production and colony formation by primary CD34⁺ MPN stem/progenitor cells from patients. Moreover, IL-33 improved the survival of JAK2^V617F-positive cell lines. Together, these data indicate a central role for IL-33 signaling in the pathogenesis of MPNs.     

Female offspring sired by diet induced obese male mice display impaired blastocyst development with molecular alterations to their ovaries,oocytes and cumulus cells

Purpose

To investigate the impacts that a paternal high fat diet (HFD) has on embryology, ovarian/cumulus cell gene expression and COC metabolism from female offspring, using a mouse model.

Methods

Founder male mice were either fed a control diet (CD) or a HFD for 12 weeks. The HFD induced obesity but not diabetes, and founder males were then mated to normal weight CD fed female mice. Female offspring were maintained on a CD, super-ovulated, mated and the resultant zygotes were cultured to the blastocyst stage for embryo morphology, blastocyst cell number and apoptosis assessment. Ovaries and cumulus cells from offspring were collected for gene expression analysis of selected genes that maintain chromatin remodeling and endoplasmic reticulum (ER), metabolic and inflammatory homeostasis. Cumulus/oocyte complexes were also investigated for glucose uptake and lipid accumulation.

Results

Female offspring sired by obese fathers produced embryos with delayed development and impaired quality, displayed increases in ovarian expression of Glut1, Glut3 and Glut4, and an increase in cumulus cell expression of Glut4. Interestingly their COCs did take up more glucose, but did accumulate more lipid.

Conclusions

A paternal HFD is associated with subfertility in female offspring despite the offspring being fed a CD and this subfertility is concomitant with ovarian/cumulus cell molecular alterations and increased lipid accumulation.

Electronic supplementary material

The online version of this article (doi:10.1007/s10815-015-0470-x) contains supplementary material, which is available to authorized users.