A supraomohyoidal plexus block designed to avoid complications

Interscalene blocks of the brachial plexus are used for surgery of the shoulder and are frequently associated with complications such as temporary phrenic block, Horner syndrome or hematoma. To minimize the risk of these complications, we developed an approach that avoids medially directed needle advancement and favors spread to lateral regions only: the supraomohyoidal block. We tested this procedure in 11 cadavers fixed by Thiel's method. The insertion site is at the lateral margin of the sternocleidomastoid muscle at the level of the cricoid cartilage. The needle is inserted in the axis of the plexus with an angle of approximately 35° to the skin, and advanced in lateral and caudal direction. Distribution of solution was determined in ten cadavers after bilateral injection of colored solution (20 and 30ml) and followed by dissection. In an eleventh cadaver, computerized tomography and 3D reconstruction after radio contrast injection was performed. In additional five cadavers we performed Winnie's technique with bilateral injection (20 and 30ml).Concerning the supraomohyoidal block the injection mass reached the infraclavicular region surrounded all trunks of the brachial plexus in the supraclavicular region and the suprascapular nerve in all cases. The solution did not spread medially beyond the lateral margin of the anterior scalene muscle into the scalenovertebral triangle. Therefore, phrenic nerve, stellate ganglion, laryngeal nerve nor the vertebral artery were exposed to the injected solution. Distribution was comparable with the use of 20 and 30ml of solution. Injections on five cadavers performing the interscalene block of Winnie resulted in an extended spread medially to the anterior scalene muscle.We conclude that our method may be a preferred approach due to its safety, because no structures out of interest were reached. Solution of 20ml is suggested to be enough for a successful bloc

A model for archaeologically relevant Holocene climate impacts in the Aegean-Levantine region (easternmost Mediterranean)

A repeating pattern of multi-centennial-scale Holocene climate events has been widely (globally) documented, and they were termed Rapid Climate Change (RCC) events. Non-seasalt potassium ion (K+) series in Greenland ice cores provide well-constrained timings for the events, and a direct timing relationship has been inferred between these events and the frequency of northerly cold polar/continental air outbreaks over the eastern Mediterranean Sea through gaps in the mountain ranges along the northern margin of the basin. There also appears to be a remarkable timing agreement with major archaeological turnover events in the Aegean/Levantine region. Yet no physically consistent assessment exists for understanding the regional climatic impacts of the events around this critical region. We present a simple 2-dimensional Lagrangian model, which yields a broad suite of physically coherent simulations of the impacts of frequency changes in winter-time northerly air outbreaks over the Aegean/Levantine region. We validate this with existing reconstructions from palaeoclimate proxy data, with emphasis on well-validated sea-surface temperature reconstructions and a highly resolved cave speleothem stable oxygen isotope record from Lebanon. Given that the RCCs were clearly marked by negative sea surface temperature anomalies in the region, we find that the predominant climatic impacts of this winter-time mechanism were “cold and wet,” in contrast with intercalated “warmer and more arid” conditions of non-RCC periods. More specifically, the RCCs are found to be periods of highly variable conditions, with an overall tendency toward cold and wet conditions with potential for flash flooding and for episodic snow-cover at low altitudes, at least in the lower-altitude (lower 1–1.5 km) regions of Crete and the Levant. The modelled winter-anomaly process cannot address underlying longer-term, astronomically forced trends, or the relatively warm and arid anomalies in between RCCs. The latter require further study, for example with respect to potential (summer-time?) extension of evaporative subtropical conditions over the region. Finally, our results imply that the “amount effect” observed in Levantine cave δ18O (and precipitation or drip-water δ18O) may not reflect the conventional concept related to temperature-dependent fractionation and Rayleigh distillation. Instead, it appears to arise from a complex and somewhat counter-intuitive mixing, in shifting proportionalities, between advected (external) and evaporated (Mediterranean) moisture.Australian Laureate Fellowship | Ref. FL120100050Universidade de Vig

CXCL12 Mediates CCR7-independent Homing of Central Memory Cells, But Not Naive T Cells, in Peripheral Lymph Nodes

Central memory CD8+ T cells (TCM) confer superior protective immunity against infections compared with other T cell subsets. TCM recirculate mainly through secondary lymphoid organs, including peripheral lymph nodes (PLNs). Here, we report that TCM, unlike naive T cells, can home to PLNs in both a CCR7-dependent and -independent manner. Homing experiments in paucity of lymph node T cells (plt/plt) mice, which do not express CCR7 ligands in secondary lymphoid organs, revealed that TCM migrate to PLNs at ∼20% of wild-type (WT) levels, whereas homing of naive T cells was reduced by 95%. Accordingly, a large fraction of endogenous CD8+ T cells in plt/plt PLNs displayed a TCM phenotype. Intravital microscopy of plt/plt subiliac lymph nodes showed that TCM rolled and firmly adhered (sticking) in high endothelial venules (HEVs), whereas naive T cells were incapable of sticking. Sticking of TCM in plt/plt HEVs was pertussis toxin sensitive and was blocked by anti-CXCL12 (SDF-1α). Anti-CXCL12 also reduced homing of TCM to PLNs in WT animals by 20%, indicating a nonredundant role for this chemokine in the presence of physiologic CCR7 agonists. Together, these data distinguish naive T cells from TCM, whereby only the latter display greater migratory flexibility by virtue of their increased responsiveness to both CCR7 ligands and CXCL12 during homing to PLN

Differential criterion of a bubble collapse in viscous liquids

The present work is devoted to a model of bubble collapse in a Newtonian viscous liquid caused by an initial bubble wall motion. The obtained bubble dynamics described by an analytic solution significantly depends on the liquid and bubble parameters. The theory gives two types of bubble behavior: collapse and viscous damping. This results in a general collapse condition proposed as the sufficient differential criterion. The suggested criterion is discussed and successfully applied to the analysis of the void and gas bubble collapses.Comment: 5 pages, 3 figure

Cutaneous Immune Cell-Microbiota Interactions Are Controlled by Epidermal JunB/AP-1

Atopic dermatitis (AD) is a multi-factorial skin disease with a complex inflammatory signature including type 2 and type 17 activation. Although colonization by S. aureus is common in AD, the mechanisms rendering an organism prone to dysbiosis, and the role of IL-17A in the control of S. aureus-induced skin inflammation, are not well understood. Here, we show several pathological aspects of AD, including type 2/type 17 immune responses, elevated IgE, barrier dysfunction, pruritus, and importantly, spontaneous S. aureus colonization in JunBΔep mice, with a large transcriptomic overlap with AD. Additionally, using Rag1-/- mice, we demonstrate that adaptive immune cells are necessary for protection against S. aureus colonization. Prophylactic antibiotics, but not antibiotics after established dysbiosis, reduce IL-17A expression and skin inflammation, examined using Il17a-eGFP reporter mice. Mechanistically, keratinocytes lacking JunB exhibit higher MyD88 levels in vitro and in vivo, previously shown to regulate S. aureus colonization. In conclusion, our data identify JunB as an upstream regulator of microbiota-immune cell interactions and characterize the IL-17A response upon spontaneous dysbiosis.We thank the Wagner lab for helpful suggestions and discussion throughout the evolution of this project, specifically Alvaro Ucero, Nuria Gago, and Liliana Mellor. We thank Vanessa Bermeo and Guillermo Medrano for help with animal husbandry and genotyping. O.U. was funded by the ECTS/Amgen Bone Biology Fellowship (2013-2016) and by the Spanish Ministry of Economy and Competitiveness (SAF2012-39670). B.R. and W.W. were funded by a Jesus-Serra visiting scientist grant. E.F.W. was funded by a European Research Council advanced grant (ERC FCK/2008/37).S

An Alternative Method to Deduce Bubble Dynamics in Single Bubble Sonoluminescence Experiments

In this paper we present an experimental approach that allows to deduce the important dynamical parameters of single sonoluminescing bubbles (pressure amplitude, ambient radius, radius-time curve) The technique is based on a few previously confirmed theoretical assumptions and requires the knowledge of quantities such as the amplitude of the electric excitation and the phase of the flashes in the acoustic period. These quantities are easily measurable by a digital oscilloscope, avoiding the cost of expensive lasers, or ultrafast cameras of previous methods. We show the technique on a particular example and compare the results with conventional Mie scattering. We find that within the experimental uncertainties these two techniques provide similar results.Comment: 8 pages, 5 figures, submitted to Phys. Rev.

CCN3 controls 3D spatial localization of melanocytes in the human skin through DDR1

Melanocytes reside within the basal layer of the human epidermis, where they attach to the basement membrane and replicate at a rate proportionate to that of keratinocytes, maintaining a lifelong stable ratio. In this study, we report that coculturing melanocytes with keratinocytes up-regulated CCN3, a matricellular protein that we subsequently found to be critical for the spatial localization of melanocytes to the basement membrane. CCN3 knockdown cells were dissociated either upward to the suprabasal layers of the epidermis or downward into the dermis. The overexpression of CCN3 increased adhesion to collagen type IV, the major component of the basement membrane. As the receptor responsible for CCN3-mediated melanocyte localization, we identified discoidin domain receptor 1 (DDR1), a receptor tyrosine kinase that acts as a collagen IV adhesion receptor. DDR1 knockdown decreased melanocyte adhesion to collagen IV and shifted melanocyte localization in a manner similar to CCN3 knockdown. These results demonstrate an intricate and necessary communication between keratinocytes and melanocytes in maintaining normal epidermal homeostasis