Astrocytes evoke a robust IRF7-independent type I interferon response upon neurotropic viral infection.

BACKGROUND: Type I interferons (IFN-I) are fundamental in controlling viral infections but fatal interferonopathy is restricted in the immune-privileged central nervous system (CNS). In contrast to the well-established role of Interferon Regulatory Factor 7 (IRF7) in the regulation of IFN-I response in the periphery, little is known about the specific function in the CNS. METHODS: To investigate the role for IRF7 in antiviral response during neurotropic virus infection, mice deficient for IRF3 and IRF7 were infected systemically with Langat virus (LGTV). Viral burden and IFN-I response was analyzed in the periphery and the CNS by focus formation assay, RT-PCR, immunohistochemistry and in vivo imaging. Microglia and infiltration of CNS-infiltration of immune cells were characterized by flow cytometry. RESULTS: Here, we demonstrate that during infection with the neurotropic Langat virus (LGTV), an attenuated member of the tick-borne encephalitis virus (TBEV) subgroup, neurons do not rely on IRF7 for cell-intrinsic antiviral resistance and IFN-I induction. An increased viral replication in IRF7-deficient mice suggests an indirect antiviral mechanism. Astrocytes rely on IRF7 to establish a cell-autonomous antiviral response. Notably, the loss of IRF7 particularly in astrocytes resulted in a high IFN-I production. Sustained production of IFN-I in astrocytes is independent of an IRF7-mediated positive feedback loop. CONCLUSION: IFN-I induction in the CNS is profoundly regulated in a cell type-specific fashion.

Fabrication of Single-Crystalline CoCrFeNi Thin Films by DC Magnetron Sputtering: A Route to Surface Studies of High-Entropy Alloys.

High-entropy alloys (HEAs) with their almost limitless number of possible compositions have raised widespread attention in material science. Next to wear and corrosion resistive coatings, their application as tunable electrocatalysts has recently moved into the focus. On the other hand, fundamental properties of HEA surfaces like atomic and electronic structure, surface segregation and diffusion as well as adsorption on HEA surfaces are barely explored. The lack of research is caused by the limited availability of single-crystalline samples. In the present work, the epitaxial growth of face centered cubic (fcc) CoCrFeNi films on MgO(100) is reported. Their characterization by X-ray diffraction (XRD), energy dispersive X-ray spectroscopy (EDX), and transmission electron microscopy (TEM) demonstrates that the layers with a homogeneous and close to equimolar elemental composition are oriented in [100] direction and aligned with the substrate to which they form an abrupt interface. X-ray photoelectron spectroscopy (XPS), low-energy electron diffraction (LEED), and angle-resolved photoelectron spectroscopy are employed to study chemical composition and atomic and electronic structure of CoCrFeNi(100). It is demonstrated that epitaxially grown HEA films have the potential to fill the sample gap, allowing for fundamental studies of properties of and processes on well-defined HEA surfaces over the full compositional space.

Deletion of p75NTR rescues the synaptic but not the inflammatory status in the brain of a mouse model for Alzheimer's disease.

Introduction: Alzheimer's disease (AD), is characterized by a gradual cognitive decline associated with the accumulation of Amyloid beta (Aß)-oligomers, progressive neuronal degeneration and chronic neuroinflammation. Among the receptors shown to bind and possibly transduce the toxic effects of Aß-oligomers is the p75 neurotrophin receptor (p75NTR). Interestingly, p75NTR mediates several crucial processes in the nervous system, including neuronal survival and apoptosis, maintenance of the neuronal architecture, and plasticity. Furthermore, p75NTR is also expressed in microglia, the resident immune cells of the brain, where it is markedly increased under pathological conditions. These observations indicate p75NTR as a potential candidate for mediating Aß-induced toxic effects at the interface between the nervous and the immune system, thereby potentially participating in the crosstalk between these two systems. Methods: Here we used APP/PS1 transgenic mice (APP/PS1tg) and compared the Aß-induced alterations in neuronal function, chronic inflammation as well as their cognitive consequences between 10 months old APP/PS1tg and APP/PS1tg x p75NTRexonIV knockout mice. Results: Electrophysiological recordings show that a loss of p75NTR rescues the impairment in long-term potentiation at the Schaffer collaterals in the hippocampus of APP/PS1tg mice. Interestingly, however loss of p75NTR does not influence the severity of neuroinflammation, microglia activation or the decline in spatial learning and memory processes observed in APP/PS1tg mice. Conclusion: Together these results indicate that while a deletion of p75NTR rescues the synaptic defect and the impairment in synaptic plasticity, it does not affect the progression of the neuroinflammation and the cognitive decline in a mouse model for AD.

Experience with "Select Crowd Review" in Peer Review for The Thoracic and Cardiovascular Surgeon: 1-Year Experience.

OBJECTIVE: To evaluate the experience with a new peer review method, "Select Crowd Review" (SCR): anonymized PDFs of manuscripts are accessible to a reviewer crowd via an online platform. It has access for 10 days to enter anonymized comments directly into the manuscript. A SCR-Editor summarizes the annotations, giving a recommendation. Both reviewed PDF and summary are sent back to authors. Upon submission, authors are given a choice to accept or decline SCR. DESIGN: All manuscript submissions since introduction in July 2021 until July 2022 were analyzed regarding acceptance and quality. Manuscripts were sent to a crowd of 45 reviewers and regular double-blinded peer review at the same time. Efficiency and performance of the crowd's reviews were compared with those of regular review. For thoracic manuscripts, a crowd was not yet available. RESULTS: SCR was accepted by the authors for 73/179 manuscripts (40.8%). After desk rejections, 51 cardiac manuscripts entered SCR. For five manuscripts, the crowd did not respond. In all remaining papers, the crowd's recommendation concurred with that of the normal reviewers. Regular peer review took up to 6 weeks. Twelve manuscripts underwent repeated SCR after revision. A median of 2 (0-9) crowd members sent in reviews. In revisions, average response was one reviewer responding. CONCLUSION: SCR encountered good acceptance by authors. As the first experience showed concordant recommendations compared with traditional review, we have extended SCR to thoracic manuscripts for more experience. SCR may become the sole review method for eligible manuscripts. Efficiency should be increased, especially for re-review of revisions.

The Effect of Thumb Metacarpophalangeal Hyperextension on Thumb Axial Load and Lateral Pinch Force in a Cadaver Model of Thumb Trapeziectomy and Flexor Carpi Radialis Suspensionplasty.

PURPOSE: The purpose of our study was to investigate, in a cadaver model, the effect of increasing thumb metacarpophalangeal (MCP) joint hyperextension on thumb axial load and key pinch force after thumb trapeziectomy and flexor carpi radialis suspensionplasty. We developed a cadaveric model to test whether thumb MCP joint hyperextension after trapeziectomy would have a negative effect on key pinch force and increase loads across a reconstructed thumb carpometacarpal (CMC) joint. METHODS: We created a cadaveric biomechanical model that varied thumb MCP joint hyperextension while measuring thumb CMC axial and key pinch force under standardized loads. Direct observations were made of how key pinch and axial thumb CMC force change with increasing thumb MCP joint hyperextension. We measured the thumb key pinch force and axial thumb CMC joint load with the thumb MCP joint in 0°, 10°, 20°, 30°, 40°, 50°, and 60° of hyperextension. RESULTS: There was a 0.88 N (2.4%) increase in axial force across the thumb CMC per every 10° of increasing thumb MCP joint hyperextension. We found a 0.53 N (4.4%) reduction in key pinch force for every 10° of increasing thumb MCP joint hyperextension. Therefore, at 60° of thumb MCP joint hyperextension, the axial force across the thumb CMC increased by 5.3 N (14.6%) and the key pinch force was weakened by 3.2 N (26.6%). CONCLUSIONS: With progressive thumb MCP joint hyperextension after thumb CMC arthroplasty, we found a decrease in key pinch force and an increase in axial thumb CMC joint force. The decrease in key pinch force was larger than the relatively small increase in thumb CMC force. CLINICAL RELEVANCE: This study helps elucidate the biomechanics of the thumb CMC joint after resection arthroplasty with thumb MCP joint hyperextension and helps understand the interplay between these 2 conditions.

The neuropeptide PACAP alleviates T. gondii infection-induced neuroinflammation and neuronal impairment.

BACKGROUND: Cerebral infection with the protozoan Toxoplasma gondii (T. gondii) is responsible for inflammation of the central nervous system (CNS) contributing to subtle neuronal alterations. Albeit essential for brain parasite control, continuous microglia activation and recruitment of peripheral immune cells entail distinct neuronal impairment upon infection-induced neuroinflammation. PACAP is an endogenous neuropeptide known to inhibit inflammation and promote neuronal survival. Since PACAP is actively transported into the CNS, we aimed to assess the impact of PACAP on the T. gondii-induced neuroinflammation and subsequent effects on neuronal homeostasis. METHODS: Exogenous PACAP was administered intraperitoneally in the chronic stage of T. gondii infection, and brains were isolated for histopathological analysis and determination of pathogen levels. Immune cells from the brain, blood, and spleen were analyzed by flow cytometry, and the further production of inflammatory mediators was investigated by intracellular protein staining as well as expression levels by RT-qPCR. Neuronal and synaptic alterations were assessed on the transcriptional and protein level, focusing on neurotrophins, neurotrophin-receptors and signature synaptic markers. RESULTS: Here, we reveal that PACAP administration reduced the inflammatory foci and the number of apoptotic cells in the brain parenchyma and restrained the activation of microglia and recruitment of monocytes. The neuropeptide reduced the expression of inflammatory mediators such as IFN-γ, IL-6, iNOS, and IL-1ß. Moreover, PACAP diminished IFN-γ production by recruited CD4+ T cells in the CNS. Importantly, PACAP promoted neuronal health via increased expression of the neurotrophin BDNF and reduction of p75NTR, a receptor related to neuronal cell death. In addition, PACAP administration was associated with increased expression of transporters involved in glutamatergic and GABAergic signaling that are particularly affected during cerebral toxoplasmosis. CONCLUSIONS: Together, our findings unravel the beneficial effects of exogenous PACAP treatment upon infection-induced neuroinflammation, highlighting the potential implication of neuropeptides to promote neuronal survival and minimize synaptic prejudice.

Type 1 innate lymphoid cells regulate the onset of Toxoplasma gondii-induced neuroinflammation.

Cerebral infections are restrained by a complex interplay of tissue-resident and recruited peripheral immune cells. Whether innate lymphoid cells (ILCs) are involved in the orchestration of the neuroinflammatory dynamics is not fully understood. Here, we demonstrate that ILCs accumulate in the cerebral parenchyma, the choroid plexus, and the meninges in the onset of cerebral Toxoplasma gondii infection. Antibody-mediated depletion of conventional natural killer (cNK) cells and ILC1s in the early stage of infection results in diminished cytokine and chemokine expression and increased cerebral parasite burden. Using cNK- and ILC1-deficient murine models, we demonstrate that exclusively the lack of ILC1s affects cerebral immune responses. In summary, our results provide evidence that ILC1s are an early source of IFN-γ and TNF in response to cerebral T. gondii infection, thereby inducing host defense factors and initiating the development of a neuroinflammatory response.

Artificial Intelligence: Its future in the health sector and its role for medical education.

The - possibly - imminent AI revolution will, to a great extent, affect the education and training for all knowledge-working professions, and therefore must be considered an important aspect also of CME. This paper reviews some of the misconceptions about AI technology, then turns to point out possible applications of AI in the medical domain and then addresses the question what this will mean for (continuing) medical education.

Influenza A Virus (H1N1) Infection Induces Microglial Activation and Temporal Dysbalance in Glutamatergic Synaptic Transmission.

Influenza A virus (IAV) causes respiratory tract disease and is responsible for seasonal and reoccurring epidemics affecting all age groups. Next to typical disease symptoms, such as fever and fatigue, IAV infection has been associated with behavioral alterations presumably contributing to the development of major depression. Previous experiments using IAV/H1N1 infection models have shown impaired hippocampal neuronal morphology and cognitive abilities, but the underlying pathways have not been fully described. In this study, we demonstrate that infection with a low-dose non-neurotrophic H1N1 strain of IAV causes ample peripheral immune response followed by a temporary blood-brain barrier disturbance. Although histological examination did not reveal obvious pathological processes in the brains of IAV-infected mice, detailed multidimensional flow cytometric characterization of immune cells uncovered subtle alterations in the activation status of microglial cells. More specifically, we detected an altered expression pattern of major histocompatibility complex classes I and II, CD80, and F4/80 accompanied by elevated mRNA levels of CD36, CD68, C1QA, and C3, suggesting evolved synaptic pruning. To closer evaluate how these profound changes affect synaptic balance, we established a highly sensitive multiplex flow cytometry-based approach called flow synaptometry. The introduction of this novel technique enabled us to simultaneously quantify the abundance of pre- and postsynapses from distinct brain regions. Our data reveal a significant reduction of VGLUT1 in excitatory presynaptic terminals in the cortex and hippocampus, identifying a subtle dysbalance in glutamatergic synapse transmission upon H1N1 infection in mice. In conclusion, our results highlight the consequences of systemic IAV-triggered inflammation on the central nervous system and the induction and progression of neuronal alterations. IMPORTANCE Influenza A virus (IAV) causes mainly respiratory tract disease with fever and fatigue but is also associated with behavioral alterations in humans. Here, we demonstrate that infection with a low-dose non-neurotrophic H1N1 strain of IAV causes peripheral immune response followed by a temporary blood-brain barrier disturbance. Characterization of immune cells uncovered subtle alterations in the activation status of microglia cells that might reshape neuronal synapses. We established a highly sensitive multiplex flow cytometry-based approach called flow synaptometry to more closely study the synapses. Thus, we detected a specific dysbalance in glutamatergic synapse transmission upon H1N1 infection in mice. In conclusion, our results highlight the consequences of systemic IAV-triggered inflammation on the central nervous system and the induction and progression of neuronal alterations.

The Immunoproteasome Subunits LMP2, LMP7 and MECL-1 Are Crucial Along the Induction of Cerebral Toxoplasmosis.

Cell survival and function critically relies on the fine-tuned balance of protein synthesis and degradation. In the steady state, the standard proteasome is sufficient to maintain this proteostasis. However, upon inflammation, the sharp increase in protein production requires additional mechanisms to limit protein-associated cellular stress. Under inflammatory conditions and the release of interferons, the immunoproteasome (IP) is induced to support protein processing and recycling. In antigen-presenting cells constitutively expressing IPs, inflammation-related mechanisms contribute to the formation of MHC class I/II-peptide complexes, which are required for the induction of T cell responses. The control of Toxoplasma gondii infection relies on Interferon-γ (IFNγ)-related T cell responses. Whether and how the IP affects the course of anti-parasitic T cell responses along the infection as well as inflammation of the central nervous system is still unknown. To answer this question we used triple knockout (TKO) mice lacking the 3 catalytic subunits of the immunoproteasome (ß1i/LMP2, ß2i/MECL-1 and ß5i/LMP7). Here we show that the numbers of dendritic cells, monocytes and CD8+ T cells were reduced in Toxoplasma gondii-infected TKO mice. Furthermore, impaired IFNγ, TNF and iNOS production was accompanied by dysregulated chemokine expression and altered immune cell recruitment to the brain. T cell differentiation was altered, apoptosis rates of microglia and monocytes were elevated and STAT3 downstream signaling was diminished. Consequently, anti-parasitic immune responses were impaired in TKO mice leading to elevated T. gondii burden and prolonged neuroinflammation. In summary we provide evidence for a critical role of the IP subunits ß1i/LMP2, ß2i/MECL-1 and ß5i/LMP7 for the control of cerebral Toxoplasma gondii infection and subsequent neuroinflammation.

Attenuation of the extracellular matrix restores microglial activity during the early stage of amyloidosis.

In the advanced stages of Alzheimer's disease (AD), microglia are transformed to an activated phenotype with thickened and retracted processes, migrate to the site of amyloid-beta (Aß) plaques, and proliferate. In the early stages of AD, it is still poorly understood whether the microglial function is altered and which factors may regulate these changes. Here, we focused on studying microglia in the retrosplenial cortex (RSC) in 3- to 4-month-old 5xFAD mice as a transgenic mouse model of AD. At this age, there are neither Aß plaques, nor activation of microglia, nor dysregulation in the expression of genes encoding major extracellular matrix (ECM) molecules or extracellular proteases in the RSC. Still, histochemical evaluation of the fine structure of neural ECM revealed increased levels of Wisteria floribunda agglutinin labeling in holes of perineuronal nets and changes in the perimeter of ECM barriers around the holes in 5xFAD mice. Two-photon vital microscopy demonstrated normal morphology and resting motility of microglia but strongly diminished number of microglial cells that migrated to the photolesion site in 5xFAD mice. Enzymatic digestion of ECM by chondroitinase ABC (ChABC) ameliorated this defect. Accordingly, the characterization of cell surface markers by flow cytometry demonstrated altered expression of microglial CD45. Moreover, ChABC treatment reduced the invasion of myeloid-derived mononuclear cells into the RSC of 5xFAD mice. Hence, the migration of both microglia and myeloid cells is altered during the early stages of amyloidosis and can be restored at least partially by the attenuation of the ECM.

Treatment-resistant cough: a rare manifestation of IgG4-related disease involving the larynx.

IgG4-related autoimmune diseases (IgG4 RD) are a relatively recently recognised group of disease processes that can affect multiple organ systems and result in protean symptoms. Here, we present a rare case of a 69-year-old man with a history of IgG4 RD affecting his lacrimal gland and pancreas who developed symptoms of severe laryngitis not responsive to usual therapy. He presented with non-productive cough, hoarseness and dyspnoea. Imaging findings suggestive of aortitis and laryngeal inflammation in the setting of his IgG4 RD history prompted treatment with rituximab, which resulted in resolution of his laryngeal symptoms. Subsequently, his cough returned and he required periodic rituximab infusions to stay symptom-free. IgG4 RD of the larynx is an uncommonly reported manifestation in literature. This disease is very responsive to anti-CD20 monoclonal antibody treatment. IgG4 RD should be considered in patients with airway symptoms that are especially refractory to usual therapy.

Arthritis of the Thumb Interphalangeal and Finger Distal Interphalangeal Joint.

The distal interphalangeal (DIP) joints are subjected to the highest joint forces in the hand, and at least 60% of individuals older than age 60 years have DIP joint arthritis. Debridement of degenerative distal interphalangeal joints with mild to moderate disease can provide satisfactory outcomes; however, those joints with more severe angular and rotation changes are reliably treated with fusions. Regardless of the fixation method, DIP fusions have high success rates, are well tolerated, and are extremely durable.

Neuronal impairment following chronic Toxoplasma gondii infection is aggravated by intestinal nematode challenge in an IFN-γ-dependent manner.

BACKGROUND: It has become increasingly evident that the immune and nervous systems are closely intertwined, relying on one another during regular homeostatic conditions. Prolonged states of imbalance between neural and immune homeostasis, such as chronic neuroinflammation, are associated with a higher risk for neural damage. Toxoplasma gondii is a highly successful neurotropic parasite causing persistent subclinical neuroinflammation, which is associated with psychiatric and neurodegenerative disorders. Little is known, however, by what means neuroinflammation and the associated neural impairment can be modulated by peripheral inflammatory processes. METHODS: Expression of immune and synapse-associated genes was assessed via quantitative real-time PCR to investigate how T. gondii infection-induced chronic neuroinflammation and associated neuronal alterations can be reshaped by a subsequent acute intestinal nematode co-infection. Immune cell subsets were characterized via flow cytometry in the brain of infected mice. Sulfadiazine and interferon-γ-neutralizing antibody were applied to subdue neuroinflammation. RESULTS: Neuroinflammation induced by T. gondii infection of mice was associated with increased microglia activation, recruitment of immune cells into the brain exhibiting Th1 effector functions, and enhanced production of Th1 and pro-inflammatory molecules (IFN-γ, iNOS, IL-12, TNF, IL-6, and IL-1ß) following co-infection with Heligmosomoides polygyrus. The accelerated cerebral Th1 immune response resulted in enhanced T. gondii removal but exacerbated the inflammation-related decrease of synapse-associated gene expression. Synaptic proteins EAAT2 and GABAAα1, which are involved in the excitation/inhibition balance in the CNS, were affected in particular. These synaptic alterations were partially recovered by reducing neuroinflammation indirectly via antiparasitic treatment and especially by application of IFN-γ-neutralizing antibody. Impaired iNOS expression following IFN-γ neutralization directly affected EAAT2 and GABAAα1 signaling, thus contributing to the microglial regulation of neurons. Besides, reduced CD36, TREM2, and C1qa gene expression points toward inflammation induced synaptic pruning as a fundamental mechanism. CONCLUSION: Our results suggest that neuroimmune responses following chronic T. gondii infection can be modulated by acute enteric nematode co-infection. While consecutive co-infection promotes parasite elimination in the CNS, it also adversely affects gene expression of synaptic proteins, via an IFN-γ-dependent manner.

Immunomodulatory Effects of the Neuropeptide Pituitary Adenylate Cyclase-Activating Polypeptide in Acute Toxoplasmosis.

Pituitary Adenylate Cyclase-Activating Polypeptide (PACAP) is an endogenous neuropeptide with distinct functions including the regulation of inflammatory processes. PACAP is able to modify the immune response by directly regulating macrophages and monocytes inhibiting the production of inflammatory cytokines, chemokines and free radicals. Here, we analyzed the effect of exogenous PACAP on peripheral immune cell subsets upon acute infection with the parasite Toxoplasma gondii (T. gondii). PACAP administration was followed by diminished innate immune cell recruitment to the peritoneal cavity of T. gondii-infected mice. PACAP did not directly interfere with parasite replication, instead, indirectly reduced parasite burden in mononuclear cell populations by enhancing their phagocytic capacity. Although proinflammatory cytokine levels were attenuated in the periphery upon PACAP treatment, interleukin (IL)-10 and Transforming growth factor beta (TGF-ß) remained stable. While PACAP modulated VPAC1 and VPAC2 receptors in immune cells upon binding, it also increased their expression of brain-derived neurotrophic factor (BDNF). In addition, the expression of p75 neurotrophin receptor (p75NTR) on Ly6Chi inflammatory monocytes was diminished upon PACAP administration. Our findings highlight the immunomodulatory effect of PACAP on peripheral immune cell subsets during acute Toxoplasmosis, providing new insights about host-pathogen interaction and the effects of neuropeptides during inflammation.

p75NTR regulates brain mononuclear cell function and neuronal structure in Toxoplasma infection-induced neuroinflammation.

Neurotrophins mediate neuronal growth, differentiation, and survival via tropomyosin receptor kinase (Trk) or p75 neurotrophin receptor (p75NTR ) signaling. The p75NTR is not exclusively expressed by neurons but also by certain immune cells, implying a role for neurotrophin signaling in the immune system. In this study, we investigated the effect of p75NTR on innate immune cell behavior and on neuronal morphology upon chronic Toxoplasma gondii (T. gondii) infection-induced neuroinflammation. Characterization of the immune cells in the periphery and central nervous system (CNS) revealed that innate immune cell subsets in the brain upregulated p75NTR upon infection in wild-type mice. Although cell recruitment and phagocytic capacity of p75NTRexonIV knockout (p75-/- ) mice were not impaired, the activation status of resident microglia and recruited myeloid cell subsets was altered. Importantly, recruited mononuclear cells in brains of infected p75-/- mice upregulated the production of the cytokines interleukin (IL)-10, IL-6 as well as IL-1α. Protein levels of proBDNF, known to negatively influence neuronal morphology by binding p75NTR , were highly increased upon chronic infection in the brain of wild-type and p75-/- mice. Moreover, upon infection the activated immune cells contributed to the proBDNF release. Notably, the neuroinflammation-induced changes in spine density were rescued in the p75-/- mice. In conclusion, these findings indicate that neurotrophin signaling via the p75NTR affects innate immune cell behavior, thus, influencing the structural plasticity of neurons under inflammatory conditions.

Platelet-rich plasma in the foot and ankle.

PURPOSE OF REVIEW: Platelet-rich plasma has become an increasingly popular treatment option within the orthopedic community to biologically enhance and stimulate difficult-to-heal musculoskeletal tissues. This review evaluates the recent literature on platelet-rich plasma use in the treatment of foot and ankle pathologies. RECENT FINDINGS: Recent literature has demonstrated platelet-rich plasma to have a possible benefit in the treatment of Achilles pathology, chronic plantar fasciitis, osteochondral lesions of the talus, ankle osteoarthritis, and diabetic foot ulcers. However, given the lack of standardization of platelet-rich plasma preparations and protocols and the predominance of low-quality studies, no definitive treatment indications exist. Platelet-rich plasma is a promising treatment option, but at present, there is only limited clinical evidence supporting its use in foot and ankle applications.

Exploring Possibilities for Transforming Established Subscription-based Scientific Journals into Open Access Journals. Present Situation, Transformation Criteria, and Exemplary Implementation within Trans-O-MIM.

BACKGROUND: Based on today's information and communication technologies the open access paradigm has become an important approach for adequately communicating new scientific knowledge. OBJECTIVES: Summarizing the present situation for journal transformation. Presenting criteria for adequate transformation as well as a specific approach for it. Describing our exemplary implementation of such a journal transformation. METHODS: Studying the respective literature as well as discussing this topic in various discussion groups and meetings (primarily of editors and publishers, but also of authors and readers), with long term experience as editors and /or publishers of scientific publications as prerequisite. RESULTS: There is a clear will, particularly of political and funding organizations, towards open access publishing. In spite of this, there is still a large amount of scientific knowledge, being communicated through subscription-based journals. For successfully transforming such journals into open access, sixteen criteria for a goal-oriented, stepwise, sustainable, and fair transformation are suggested. The Tandem Model as transformation approach is introduced. Our exemplary implementation is done in the Trans-O-MIM project. It is exploring strategies, models and evaluation metrics for journal transformation. As instance the journal Methods of Information in Medicine will apply the Tandem Model from 2017 onwards. CONCLUSIONS: Within Trans-O-MIM we will reach at least nine of the sixteen criteria for adequate transformation. It was positive to implement Trans-O-MIM as international research project. After first steps for transforming Methods have successfully been made, challenges will remain, among others, in identifying appropriate incentives for open access publishing in order to support its transformation.

Correlation of Postoperative Position of the Sesamoids After Chevron Osteotomy With Outcome.

BACKGROUND: Postoperative incomplete reduction of the sesamoids has been identified as a potential risk factor for hallux valgus recurrence after proximal osteotomy. However, it is not known whether the postoperative sesamoid position is a risk factor in hallux valgus correction via distal chevron osteotomy with or without dorsal webspace release (DWSR). METHODS: In this retrospective study, 169 patients who underwent distal chevron osteotomy with or without DWSR were reviewed. Preoperative and postoperative (6 weeks, 6 months, 12 months) weightbearing radiographs were evaluated. Functional hallux valgus angle (HVA), intermetatarsal angle (IMA), and the position of the tibial sesamoid were graded using the center of head method. Seventy-six radiographs were available for review at the 12-month follow-up. Of these, 41 patients underwent DWSR procedure and 35 did not. RESULTS: In both groups, correction of all 3 parameters (HVA, IMA, tibial sesamoid position) were significant at the 12-month follow-up. Comparison of the postoperative results of the 2 groups showed no statistically significant differences. Four feet demonstrated displaced sesamoid position at the 12-month follow-up, with radiographic evidence of recurrence in just one. No significant relationship was found between postoperative sesamoid position and hallux valgus recurrence that occurred in 4 feet. CONCLUSION: Combining DWSR with a distal chevron osteotomy did not delay healing or increase risk of avascular necrosis, but it did not significantly improve angular measurements or sesamoid position. The concept that postoperative sesamoid position can be used to predict hallux valgus recurrence was not supported by our results when looking at distal chevron correction. LEVEL OF EVIDENCE: Level III, retrospective comparative study.