Nanoscale Magnetic Domains in Polycrystalline Mn3Sn Films Imaged by a Scanning Single-Spin Magnetometer.

Noncollinear antiferromagnets with novel magnetic orders, vanishingly small net magnetization, and exotic spin related properties hold enormous promise for developing next-generation, transformative spintronic applications. A major ongoing research focus of this community is to explore, control, and harness unconventional magnetic phases of this emergent material system to deliver state-of-the-art functionalities for modern microelectronics. Here we report direct imaging of magnetic domains of polycrystalline Mn3Sn films, a prototypical noncollinear antiferromagnet, using nitrogen-vacancy-based single-spin scanning microscopy. Nanoscale evolution of local stray field patterns of Mn3Sn samples are systematically investigated in response to external driving forces, revealing the characteristic "heterogeneous" magnetic switching behaviors in polycrystalline textured Mn3Sn films. Our results contribute to a comprehensive understanding of inhomogeneous magnetic orders of noncollinear antiferromagnets, highlighting the potential of nitrogen-vacancy centers to study microscopic spin properties of a broad range of emergent condensed matter systems.

Quantum Imaging of Magnetic Phase Transitions and Spin Fluctuations in Intrinsic Magnetic Topological Nanoflakes.

Topological materials featuring exotic band structures, unconventional current flow patterns, and emergent organizing principles offer attractive platforms for the development of next-generation transformative quantum electronic technologies. The family of MnBi2Te4 (Bi2Te3)n materials is naturally relevant in this context due to their nontrivial band topology, tunable magnetism, and recently discovered extraordinary quantum transport behaviors. Despite numerous pioneering studies to date, the local magnetic properties of MnBi2Te4 (Bi2Te3)n remain an open question, hindering a comprehensive understanding of their fundamental material properties. Exploiting nitrogen-vacancy (NV) centers in diamond, we report nanoscale quantum imaging of the magnetic phase transitions and spin fluctuations in exfoliated MnBi4Te7 flakes, revealing the underlying spin transport physics and magnetic domains at the nanoscale. Our results highlight the unique advantage of NV centers in exploring the magnetic properties of emergent quantum materials, opening new opportunities for investigating the interplay between topology and magnetism.

Strong Correlation Between Superconductivity and Ferromagnetism in an Fe-Chalcogenide Superconductor.

The interplay among topology, superconductivity, and magnetism promises to bring a plethora of exotic and unintuitive behaviors in emergent quantum materials. The family of Fe-chalcogenide superconductors FeTexSe1-x are directly relevant in this context due to their intrinsic topological band structure, high-temperature superconductivity, and unconventional pairing symmetry. Despite enormous promise and expectation, the local magnetic properties of FeTexSe1-x remain largely unexplored, which prevents a comprehensive understanding of their underlying material properties. Exploiting nitrogen vacancy (NV) centers in diamond, here we report nanoscale quantum sensing and imaging of magnetic flux generated by exfoliated FeTexSe1-x flakes, demonstrating strong correlation between superconductivity and ferromagnetism in FeTexSe1-x. The coexistence of superconductivity and ferromagnetism in an established topological superconductor opens up new opportunities for exploring exotic spin and charge transport phenomena in quantum materials. The demonstrated coupling between NV centers and FeTexSe1-x may also find applications in developing hybrid architectures for next-generation, solid-state-based quantum information technologies.

Supernatants and lipids from stored red blood cells activate pulmonary microvascular endothelium through the BLT2 receptor and protein kinase C activation.

BACKGROUND: Although transfusion is a lifesaving intervention, it may be associated with significant morbidity in injured patients. We hypothesize that stored red blood cells (RBCs) induce proinflammatory activation of human pulmonary microvascular endothelial cells (HMVECs) resulting in neutrophil (PMN) adhesion and predisposition to acute lung injury (ALI). STUDY DESIGN AND METHODS: Ten units of RBCs were collected; 50% (by weight) were leukoreduced (LR-RBCs) and the remainder was unmodified and stored in additive solution-5 (AS-5). An additional 10 units of RBCs were collected, leukoreduced, and stored in AS-3. HMVECs were incubated with [10%-40%]FINAL of the supernatants on Day (D)1 to D42 of storage, lipid extracts, and purified lipids. Endothelial surface expression of intercellular adhesion molecule-1 (ICAM-1), interleukin (IL)-8 release, and PMN adhesion to HMVECs were measured. HMVEC signaling via the BLT2 receptor was evaluated. Supernatants and lipids were also employed as the first event in a two-event model of ALI. RESULTS: The supernatants [10%-40%]FINAL from D21 LR-RBCs and D42 RBCs and LR-RBCs and the lipids from D42 stored in AS-5 induced increased ICAM-1 surface expression on endothelium, IL-8 release, and PMN adhesion. In addition, the supernatants [20%-40%]FINAL from D21 and D42 RBCs in AS-5 also increased endothelial surface expression of ICAM-1. D42 supernatants and lipids also caused coprecipitation of ß-arrestin-1 with BLT2, protein kinase C (PKC)ßI , and PKCδ and served as the first event in a two-event rodent model of ALI. CONCLUSION: Lipids that accumulate during RBC storage activate endothelium and predispose to ALI, which may explain some of the adverse events associated with the transfusion of critically injured patients.

Machine learning enabled multiplex detection of periodontal pathogens by surface-enhanced Raman spectroscopy.

Periodontitis is a chronic inflammation of the periodontium caused by a persistent bacterial infection, resulting in destruction of the supporting structures of teeth. Analysis of microbial composition in saliva can inform periodontal status. Actinobacillus actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg), and Streptococcus mutans (Sm) are among reported periodontal pathogens, and were used as model systems in this study. Our atomic force microscopic (AFM) study revealed that these pathogens are biological nanorods with dimensions of 0.6-1.1 µm in length and 500-700 nm in width. Current bacterial detection methods often involve complex preparation steps and require labeled reporting motifs. Employing surface-enhanced Raman spectroscopy (SERS), we revealed cell-type specific Raman signatures of these pathogens for label-free detection. It overcame the complexity associated with spectral overlaps among different bacterial species, relying on high signal-to-noise ratio (SNR) spectra carefully collected from pure species samples. To enable simple, rapid, and multiplexed detection, we harnessed advanced machine learning techniques to establish predictive models based on a large set of raw spectra of each bacterial species and their mixtures. Using these models, given a raw spectrum collected from a bacterial suspension, simultaneous identification of all three species in the test sample was achieved at 95.6 % accuracy. This sensing modality can be applied to multiplex detection of a broader range and a larger set of periodontal pathogens, paving the way for hassle-free detection of oral bacteria in saliva with little to no sample preparation.

Observation of stacking engineered magnetic phase transitions within moiré supercells of twisted van der Waals magnets.

Recent demonstrations of moiré magnetism, featuring exotic phases with noncollinear spin order in the twisted van der Waals (vdW) magnet chromium triiodide CrI3, have highlighted the potential of twist engineering of magnetic (vdW) materials. However, the local magnetic interactions, spin dynamics, and magnetic phase transitions within and across individual moiré supercells remain elusive. Taking advantage of a scanning single-spin magnetometry platform, here we report observation of two distinct magnetic phase transitions with separate critical temperatures within a moiré supercell of small-angle twisted double trilayer CrI3. By measuring temperature-dependent spin fluctuations at the coexisting ferromagnetic and antiferromagnetic regions in twisted CrI3, we explicitly show that the Curie temperature of the ferromagnetic state is higher than the Néel temperature of the antiferromagnetic one by ~10 K. Our mean-field calculations attribute such a spatial and thermodynamic phase separation to the stacking order modulated interlayer exchange coupling at the twisted interface of moiré superlattices.

Genome-wide analysis of the p53 gene regulatory network in the developing mouse kidney.

Despite mounting evidence that p53 senses and responds to physiological cues in vivo, existing knowledge regarding p53 function and target genes is largely derived from studies in cancer or stressed cells. Herein we utilize p53 transcriptome and ChIP-Seq (chromatin immunoprecipitation-high throughput sequencing) analyses to identify p53 regulated pathways in the embryonic kidney, an organ that develops via mesenchymal-epithelial interactions. This integrated approach allowed identification of novel genes that are possible direct p53 targets during kidney development. We find the p53-regulated transcriptome in the embryonic kidney is largely composed of genes regulating developmental, morphogenesis, and metabolic pathways. Surprisingly, genes in cell cycle and apoptosis pathways account for <5% of differentially expressed transcripts. Of 7,893 p53-occupied genomic regions (peaks), the vast majority contain consensus p53 binding sites. Interestingly, 78% of p53 peaks in the developing kidney lie within proximal promoters of annotated genes compared with 7% in a representative cancer cell line; 25% of the differentially expressed p53-bound genes are present in nephron progenitors and nascent nephrons, including key transcriptional regulators, components of Fgf, Wnt, Bmp, and Notch pathways, and ciliogenesis genes. The results indicate widespread p53 binding to the genome in vivo and context-dependent differences in the p53 regulon between cancer, stress, and development. To our knowledge, this is the first comprehensive analysis of the p53 transcriptome and cistrome in a developing mammalian organ, substantiating the role of p53 as a bona fide developmental regulator. We conclude p53 targets transcriptional networks regulating nephrogenesis and cellular metabolism during kidney development.

Local Control of a Single Nitrogen-Vacancy Center by Nanoscale Engineered Magnetic Domain Wall Motion.

Effective control and readout of qubits form the technical foundation of next-generation, transformative quantum information sciences and technologies. The nitrogen-vacancy (NV) center, an intrinsic three-level spin system, is naturally relevant in this context due to its excellent quantum coherence, high fidelity of operations, and remarkable functionality over a broad range of experimental conditions. It is an active contender for the development and implementation of cutting-edge quantum technologies. Here, we report magnetic domain wall motion driven local control and measurements of the NV spin properties. By engineering the local magnetic field environment of an NV center via nanoscale reconfigurable domain wall motion, we show that NV photoluminescence, spin level energies, and coherence time can be reliably controlled and correlated to the magneto-transport response of a magnetic device. Our results highlight the electrically tunable dipole interaction between NV centers and nanoscale magnetic structures, providing an attractive platform to realize interactive information transfer between spin qubits and nonvolatile magnetic memory in hybrid quantum spintronic systems.

A two-event in vitro model of acute chest syndrome: the role of secretory phospholipase A2 and neutrophils.

BACKGROUND: Acute chest syndrome (ACS) in sickle cell disease is associated with elevation of secretory phospholipase A(2) (sPLA(2) ). We hypothesize that sPLA(2) cleaves membrane lipids from sickled red blood cells (RBCs) causing PMN-mediated endothelial cell injury (ECI) as the second event in a two-event model. METHODS: Whole blood was collected from children when in steady state or daily during admissions for vaso-occlusive pain (VOC) or ACS. The plasma and RBCs were separated, sPLA(2) levels were measured, and the RBCs were incubated with sPLA(2) . Plasma and lipids, extracted from the plasma or the supernatant of sPLA(2) -treated RBCs, were assayed for PMN priming activity and used as the second event in a model of PMN-mediated ECI. Phosphatidylserine (PS) surface expression on RBCs was quantified by flow cytometry. RESULTS: Increased sPLA(2) -IIa levels were associated with ACS. SPLA(2) -liberated lipids from VOC and the plasma, plasma lipids and sPLA(2) -liberated lipids from ACS primed PMNs and caused PMN-mediated ECI (P < 0.01). RBCs from VOC had increased in PS surface expression versus steady state. CONCLUSIONS: ACS plasma and lipids and sPLA(2) -released lipids from RBCs during VOC or ACS induce PMN-mediated ECI. VOC elicited increases in PS surface expression providing a membrane substrate for sPLA(2) lysis of sickle RBCs.

Wide field imaging of van der Waals ferromagnet Fe3GeTe2 by spin defects in hexagonal boron nitride.

Emergent color centers with accessible spins hosted by van der Waals materials have attracted substantial interest in recent years due to their significant potential for implementing transformative quantum sensing technologies. Hexagonal boron nitride (hBN) is naturally relevant in this context due to its remarkable ease of integration into devices consisting of low-dimensional materials. Taking advantage of boron vacancy spin defects in hBN, we report nanoscale quantum imaging of low-dimensional ferromagnetism sustained in Fe3GeTe2/hBN van der Waals heterostructures. Exploiting spin relaxometry methods, we have further observed spatially varying magnetic fluctuations in the exfoliated Fe3GeTe2 flake, whose magnitude reaches a peak value around the Curie temperature. Our results demonstrate the capability of spin defects in hBN of investigating local magnetic properties of layered materials in an accessible and precise way, which can be extended readily to a broad range of miniaturized van der Waals heterostructure systems.

Noninvasive measurements of spin transport properties of an antiferromagnetic insulator.

Antiferromagnetic insulators (AFIs) are of substantial interest because of their potential in the development of next-generation spintronic devices. One major effort in this emerging field is to harness AFIs for long-range spin information communication and storage. Here, we report a noninvasive method to optically access the intrinsic spin transport properties of an archetypical AFI α-Fe2O3 via nitrogen-vacancy (NV) quantum spin sensors. By NV relaxometry measurements, we successfully detect the frequency-dependent dynamic fluctuations of the spin density of α-Fe2O3 along the Néel order parameter, from which an intrinsic spin diffusion constant of α-Fe2O3 is experimentally measured in the absence of external spin biases. Our results highlight the significant opportunity offered by NV centers in diagnosing the underlying spin transport properties in a broad range of high-frequency magnetic materials such as two-dimensional magnets, spin liquids, and magnetic Weyl semimetals, which are challenging to access by the conventional measurement techniques.

Distinct roles of NR2A and NR2B cytoplasmic tails in long-term potentiation.

NMDA receptors (NMDARs) are critical mediators of activity-dependent synaptic plasticity, but the differential roles of NR2A- versus NR2B-containing NMDARs have been controversial. Here, we investigate the roles of NR2A and NR2B in long-term potentiation (LTP) in organotypic hippocampal slice cultures using RNA interference (RNAi) and overexpression, to complement pharmacological approaches. In young slices, when NR2B is the predominant subunit expressed, LTP is blocked by the NR2B-selective antagonist Ro25-6981 [R-(R,S)-alpha-(4-hydroxyphenyl)-beta-methyl-4-(phenylmethyl)-1-piperidine propranol]. As slices mature and NR2A expression rises, activation of NR2B receptors became no longer necessary for LTP induction. LTP was blocked, however, by RNAi knockdown of NR2B, and this was rescued by coexpression of an RNAi-resistant NR2B (NR2B*) cDNA. Interestingly, a chimeric NR2B subunit in which the C-terminal cytoplasmic tail was replaced by that of NR2A failed to rescue LTP, whereas the reverse chimera, NR2A channel with NR2B tail, was able to restore LTP. Thus, expression of NR2B with its intact cytoplasmic tail is required for LTP induction, at an age when channel activity of NR2B-NMDARs is not required for LTP. Overexpression of wild-type NR2A failed to rescue LTP in neurons transfected with the NR2B-RNAi construct, despite restoring NMDA-EPSC amplitude to a similar level as NR2B*. Surprisingly, an NR2A construct lacking its entire C-terminal cytoplasmic tail regained its ability to restore LTP. Together, these data suggest that the NR2B subunit plays a critical role for LTP, presumably by recruiting relevant molecules important for LTP via its cytoplasmic tail. In contrast, NR2A is not essential for LTP, and its cytoplasmic tail seems to carry inhibitory factors for LTP.

Regulation of kidney development by histone deacetylases.

There is accumulating evidence that gene expression can be regulated independently of DNA sequence changes, also called epigenetic modifications. Histone deacetylases (HDACs), a specific epigenetic group of enzymes, dynamically and reversibly removes acetyl groups from histone tails projecting from the nucleosome. Clinically, valproic acid fetopathy sheds some insight into the effects of altered HDACs on human embryonic development, since valproic acid is an antiepileptic drug and an HDAC inhibitor. The fetal anomalies include severe renal dysgenesis, supporting the role played by HDACs in human kidney development. Our recent studies have shown that HDACs regulate the transcriptional networks required for controlling the cell cycle, Wnt signaling, and the pathway upstream of the GDNF/RET signaling pathway in the developing kidney. Here, we describe novel HDAC target genes not previously implicated in renal development based on studies using genome-wide microarrays. These genes can be divided into transcription factors, modulators of matrix biology, chromatin remodelers, and DNA repair genes. We also report that HDACs are requisite for tissue-specific gene expression.

Lysophosphatidylcholines activate G2A inducing G(αi)₋1-/G(αq/)11- Ca²(+) flux, G(ßγ)-Hck activation and clathrin/ß-arrestin-1/GRK6 recruitment in PMNs.

Lyso-PCs (lysophosphatidylcholines) are a mixture of lipids that accumulate during storage of cellular blood components, have been implicated in TRALI (transfusion-related acute lung injury) and directly affect the physiology of neutrophils [PMNs (polymorphonuclear leucocytes)]. Because the G2A receptor, expressed on PMNs, has been reported to recognize lyso-PCs, we hypothesize that lyso-PC activation of G2A causes the increases in cytosolic Ca²(+) via release of G(α) and G(ßγ) subunits, kinase activation, and the recruitment of clathrin, ß-arrestin-1 and GRK6 (G-protein receptor kinase 6) to G2A for signal transduction. PMNs were isolated by standard techniques, primed with lyso-PCs for 5-180 s, and lysed for Western blot analysis, immunoprecipitation or subcellular fractionation, or fixed and smeared on to slides for digital microscopy. The results demonstrated that lyso-PCs cause rapid activation of the G2A receptor through S-phosphorylation and internalization resulting in G(αi)₋1 and G(αq/)11 release leading to increases in cytosolic Ca²(+), which was inhibited by an antibody to G2A or intracellular neutralization of these subunits. Lyso-PCs also caused the release of the G(ßγ) subunit which demonstrated a physical interaction (FRET+) with activated Hck (haemopoietic cell kinase; Tyr4¹¹). Moreover, G2A recruited clathrin, ß-arrestin-1 and GRK6: clathrin is important for signal transduction, GRK6 for receptor de-sensitization, and ß-arrestin-1 both propagates and terminates signals. We conclude that lyso-PC activation of G2A caused release of G(αi)₋1, G(αq/)11 and G(ßγ), resulting in cytosolic Ca²(+) flux, Hck activation, and recruitment of clathrin, ß-arrestin-1 and GRK6.

Recurrent Colon Cancer: Presentation With Disseminated Intravascular Coagulation From Disseminated Carcinomatosis of the Bone Marrow.

Diffuse carcinomatosis of the bone marrow (DCBM) is a rare clinical condition characterized by diffuse bone marrow involvement with hematological changes. This case study concerns a patient who presented with DCBM secondary to colon cancer with diffuse intravascular coagulation. This is a rare presentation of DCBM in colon cancer. The case study also elaborates on clinical features, pathogenesis, and therapy of this unique presentation.

Tumor necrosis factor-alpha causes release of cytosolic interleukin-18 from human neutrophils.

Neutrophils (PMNs) are a vital part of host defense and are the principal leukocyte in innate immunity. Interleukin (IL)-18 is a proinflammatory cytokine with roles in both innate and adaptive immunity. We hypothesize that PMNs contain preformed IL-18, which is released in response to specific inflammatory stimuli. Isolated PMNs were stimulated with a battery of chemoattractants (5 min to 24 h), and IL-18 release was measured. PMNs were also separated into subcellular fractions and immunoblotted with antibodies against IL-18 or were fixed and probed with antibodies to IL-18 as well as to the contents of granules, intracellular organelles, and filamentous actin (F-actin), incubated with fluorescent secondary antibodies, and examined by digital microscopy. Quiescent PMNs contained IL-18 in the cytoplasm, associated with F-actin, as determined by positive fluorescence resonance energy transfer (FRET+). In turn, TNF-alpha stimulation disrupted the association of IL-18 with F-actin, induced a FRET+ interaction of IL-18 with lipid rafts, and elicited IL-18 release. Manipulation of F-actin status confirmed the relationship between IL-18 and F-actin in resting PMNs. Consequently, incubation with monomeric IL-18 binding protein inhibited TNF-alpha-mediated priming of the PMN oxidase. We conclude that human PMNs contain IL-18 associated with F-actin in the cytoplasm and TNF-alpha stimulation causes dissociation of IL-18 from F-actin, association with lipid rafts, and extracellular release. Extracellular IL-18 participates in TNF-alpha priming of the PMN oxidase as demonstrated by inhibition with the IL-18 binding protein.

Amantadine inhibits platelet-activating factor induced clathrin-mediated endocytosis in human neutrophils.

Receptor signaling is integral for adhesion, emigration, phagocytosis, and reactive oxygen species production in polymorphonuclear neutrophils (PMNs). Priming is an important part of PMN emigration, but it can also lead to PMN-mediated organ injury in the host. Platelet-activating factor (PAF) primes PMNs through activation of a specific G protein-coupled receptor. We hypothesize that PAF priming of PMNs requires clathrin-mediated endocytosis (CME) of the PAF receptor (PAFr), and, therefore, amantadine, known to inhibit CME, significantly antagonizes PAF signaling. PMNs were isolated by standard techniques to >98% purity and tested for viability. Amantadine (1 mM) significantly inhibited the PAF-mediated changes in the cellular distribution of clathrin and the physical colocalization [fluorescence resonance energy transfer positive (FRET+)] of early endosome antigen-1 and Rab5a, known components of CME and similar to hypertonic saline, a known inhibitor of CME. Furthermore, amantadine had no effect on the PAF-induced cytosolic calcium flux; however, phosphorylation of p38 MAPK was significantly decreased. Amantadine inhibited PAF-mediated changes in PMN physiology, including priming of the NADPH oxidase and shape change with lesser inhibition of increases in CD11b surface expression and elastase release. Furthermore, rimantadine, an amantadine analog, was a more potent inhibitor of PAF priming of the N-formyl-methionyl-leucyl-phenylalanine-activated oxidase. PAF priming of PMNs requires clathrin-mediated endocytosis that is inhibited when PMNs are pretreated with either amantadine or rimantadine. Thus, amantadine and rimantadine have the potential to ameliorate PMN-mediated tissue damage in humans.

LysoPCs induce Hck- and PKCδ-mediated activation of PKCγ causing p47phox phosphorylation and membrane translocation in neutrophils.

Lysophosphatidylcholines (lysoPCs) are effective polymorphonuclear neutrophil (PMN) priming agents implicated in transfusion-related acute lung injury (TRALI). LysoPCs cause ligation of the G2A receptor, cytosolic Ca2+ flux, and activation of Hck. We hypothesize that lysoPCs induce Hck-dependent activation of protein kinase C (PKC), resulting in phosphorylation and membrane translocation of 47 kDa phagocyte oxidase protein (p47phox). PMNs, human or murine, were primed with lysoPCs and were smeared onto slides and examined by digital microscopy or separated into subcellular fractions or whole-cell lysates. Proteins were immunoprecipitated or separated by polyacrylamide gel electrophoresis and immunoblotted for proteins of interest. Wild-type (WT) and PKCγ knockout (KO) mice were used in a 2-event model of TRALI. LysoPCs induced Hck coprecipitation with PKCδ and PKCγ and the PKCδ:PKCγ complex also had a fluorescence resonance energy transfer (FRET)+ interaction with lipid rafts and Wiskott-Aldrich syndrome protein family verprolin-homologous protein 2 (WAVE2). PKCγ then coprecipitated with p47phox Immunoblotting, immunoprecipitation (IP), specific inhibitors, intracellular depletion of PKC isoforms, and PMNs from PKCγ KO mice demonstrated that Hck elicited activation/Tyr phosphorylation (Tyr311 and Tyr525) of PKCδ, which became Thr phosphorylated (Thr507). Activated PKCδ then caused activation of PKCγ, both by Tyr phosphorylation (Τyr514) and Ser phosphorylation, which induced phosphorylation and membrane translocation of p47phox In PKCγ KO PMNs, lysoPCs induced Hck translocation but did not evidence a FRET+ interaction between PKCδ and PKCγ nor prime PMNs. In WT mice, lysoPCs served as the second event in a 2-event in vivo model of TRALI but did not induce TRALI in PKCγ KO mice. We conclude that lysoPCs prime PMNs through Hck-dependent activation of PKCδ, which stimulates PKCγ, resulting in translocation of phosphorylated p47phox.

Transfusion-related acute lung injury.

Transfusion-related acute lung injury (TRALI) is a life-threatening adverse event of transfusion, which has an increasing incidence in the United States and is the leading cause of transfusion-related death. TRALI and acute lung injury (ALI) share a common clinical definition except that TRALI is temporally- and mechanistically-related to transfusion of blood or blood components. A number of different models have been proposed to explain the pathogenesis. The first is an antibody-mediated event whereby transfusion of anti-HLA, class I or class II, or anti-granulocyte antibodies into patients whose leukocytes express the cognate antigens. The antibody:antigen interaction causes complement-mediated pulmonary sequestration and activation of neutrophils (PMNs) resulting in TRALI. The second is a two-event model: the first event is the clinical condition of the patient resulting in pulmonary endothelial activation and PMN sequestration, and the second event is the transfusion of a biologic response modifier (including anti-granulocyte antibodies, lipids, and CD40 ligand) that activates these adherent PMNs resulting in endothelial damage, capillary leak, and TRALI. These hypotheses are discussed with respect to animal models and human studies that provide the experimental and clinical relevance. The definition of TRALI, patient predisposition, treatment, prevention and reporting guidelines are also examined.

Comparison of biomechanical properties of alloderm and enduragen as static facial sling biomaterials.

BACKGROUND: Static slings are one of the most commonly used surgical rehabilitation methods in the management of chronic facial paralysis. Acellular human cadaveric dermis (Alloderm; Life Cell Corp., Branchburg, NJ) is used for this purpose; however, it has variable stretching properties that may necessitate additional "tuning-up" procedure(s). Acellular porcine dermis (Enduragen; Tissue Sciences Laboratories, plc., Aldershot, U.K.) was recently introduced as a biologic implant and it is compositionally similar to Alloderm. However, no data currently exist regarding its biomechanical properties and potential use as an alternative implant to Alloderm in static facial sling procedures. OBJECTIVE: The objective of this study was to compare the biomechanical properties of Alloderm and Enduragen for static facial sling procedures in the management of the paralytic face. STUDY DESIGN: This study consisted of an in vitro prospective study in an academic medical research setting. METHODS: Same size and thickness Alloderm and Enduragen samples were tested with MTS 858 Bionix materials test system for load-to-failure, displacement under increasing and constant stress, and stiffness. RESULTS: Enduragen showed significantly less elongation under increasing stress and at the beginning of constant stress. Load-to-failure and stiffness were significantly higher in Alloderm; however, both biomaterials have adequate stiffness and load-to-failure for a static facial sling procedure. CONCLUSIONS: Enduragen may serve as another potential static facial sling material, because it stretches significantly less than Alloderm under stress. Clinical experience is needed with Enduragen to determine its potential use as a static facial sling material.