An Analysis of Volume, Length and Segmentation of Free Fibula Flap in Reconstruction of the Jaws: Investigation of Their Role on Flap Failure

Reconstruction of defects of the jaws is mainly performed via free fibula flap. An incidence of 2-21% of overall flap failure is still described. We investigated the roles of volume, length and number of fibula flap segments on flap survival using novel three-dimensional segmentation tools. We also analyzed the role of other possible risk factors. Seventy-one consecutive patients with a follow up of at least three months and who underwent free fibula flap reconstruction in a single center between 2002 and 2022 have been evaluated. A total of 166 fibula segments were analyzed. Malignancies were the main reason of resection (45.1%). In 69% of the cases a reconstruction of the mandible was performed. The flaps were mainly divided in two segments (39%) (range 1-4), with a mean length of 2.52 cm and a mean volume was 3.37 cm(3). Total flap failure (TFF) occurred in 12 cases, (16.9%), while partial flap failure (PFF) appeared in 3 patients (4.2%). Volume, length and number of fibula flap segments did not seem to influence flap failure incidence in uni- and multivariate analysis. Reconstruction of the maxilla and use of a recipient vessel different from the facial artery seemed to significantly impact on flap failure. Smoking and previous surgeries showed a higher trend to flap failure, but they did not reach statistical significance. Prospective and multicentric analysis on a wider population should be assessed

Surgical treatment of pressure injuries in children: A multicentre experience

Pressure injuries (PI) are infrequent in paediatric patients, prevalence estimates ranging from 1.4% to 8.2%, and reaching values as high as 43.1% in critical care areas. They can be associated with congenital neurological or metabolic disorders that cause reduced mobility or require the need for medical devices. In children, most pressure injuries heal spontaneously. However, a small percentage of ulcers that is refractory to conservative management or is too severe at presentation (Stage 3 or 4) will be candidates for surgery. We retrospectively reviewed the clinical history of paediatric patients affected by pressure injuries from four European Plastic Surgery Centres. Information was collected from clinical and radiology records, and laboratory reports. An accurate search of the literature revealed only two articles reporting on the surgical treatment of pressure injuries in children. After debridement, we performed surgical coverage of the pressure injuries. We report here our experience with 18 children aged 1-17 years, affected by pressure injury Stages 3 and 4. They were successfully treated with pedicled (17 patients) or free flaps (1 patient). The injuries involved the sacrum (6/18 patients), lower limb (3/18 patients), thoracic spine (2/18 patients), ischium (3/18 patients, bilateral in one patient), temporal area (3/18 patients), hypogastrium (1/18 patients) and were associated to medical devices in three cases. Flaps were followed for a minimum of 19 months and up to 13 years. Only two patients developed true recurrences that were treated again surgically. Pressure injuries are infrequent in children and rarely need surgical treatment. Pedicled flaps have a high success rate. Recurrences, contrary to what is reported in the literature, were rare

Case Report: Could Hennebert's Sign Be Evoked Despite Global Vestibular Impairment on Video Head Impulse Test? Considerations Upon Pathomechanisms Underlying Pressure-Induced Nystagmus due to Labyrinthine Fistula

We describe a case series of labyrinthine fistula, characterized by Hennebert's sign (HS) elicited by tragal compression despite global hypofunction of semicircular canals (SCs) on a video-head impulse test (vHIT), and review the relevant literature. All three patients presented with different amounts of cochleo-vestibular loss, consistent with labyrinthitis likely induced by labyrinthine fistula due to different temporal bone pathologies (squamous cell carcinoma involving the external auditory canal in one case and middle ear cholesteatoma in two cases). Despite global hypofunction on vHIT proving impaired function for each SC for high accelerations, all patients developed pressure-induced nystagmus, presumably through spared and/or recovered activity for low-velocity canal afferents. In particular, two patients with isolated horizontal SC fistula developed HS with ipsilesional horizontal nystagmus due to resulting excitatory ampullopetal endolymphatic flows within horizontal canals. Conversely, the last patient with bony erosion involving all SCs developed mainly torsional nystagmus directed contralaterally due to additional inhibitory ampullopetal flows within vertical canals. Moreover, despite impaired measurements on vHIT, we found simultaneous direction-changing positional nystagmus likely due to a buoyancy mechanism within the affected horizontal canal in a case and benign paroxysmal positional vertigo involving the dehiscent posterior canal in another case. Based on our findings, we might suggest a functional dissociation between high (impaired) and low (spared/recovered) accelerations for SCs. Therefore, it could be hypothesized that HS in labyrinthine fistula might be due to the activation of regular ampullary fibers encoding low-velocity inputs, as pressure-induced nystagmus is perfectly aligned with the planes of dehiscent SCs in accordance with Ewald's laws, despite global vestibular impairment on vHIT. Moreover, we showed how pressure-induced nystagmus could present in a rare case of labyrinthine fistulas involving all canals simultaneously. Nevertheless, definite conclusions on the genesis of pressure-induced nystagmus in our patients are prevented due to the lack of objective measurements of both low-acceleration canal responses and otolith function

Case Report: Filling Defect in Posterior Semicircular Canal on MRI With Balanced Steady-State Gradient-Echo Sequences After Labyrinthine Ischemia in the Common Cochlear Artery Territory as an Early Sign of Fibrosis

We describe a rare case of posterior semicircular canal (PSC) fibrosis following acute labyrinthine ischemia in the territory supplied by the common cochlear artery (CCA) and review the relevant literature. A 71-year-old man with multiple vascular risk factors presented 12 days after the onset of acute vertigo and profound left-sided hearing loss. Right-beating spontaneous nystagmus with downbeat components elicited by mastoid vibrations and headshaking was detected. The video head impulse test (vHIT) revealed an isolated hypofunction of the left PSC, whereas vestibular evoked myogenic potentials (VEMPs) showed ipsilateral saccular loss. The clinical presentation and instrumental picture were consistent with acute ischemia in the territory supplied by left CCA. Compared to previous imaging, a new MRI of the brain with 3D-FIESTA sequences highlighted a filling defect in the left PSC, consistent with fibrosis. Hearing function exhibited mild improvement after steroid therapy and hyperbaric oxygen sessions, whereas vHIT abnormalities persisted over time. To the best of our knowledge, this is the only case in the literature reporting a filling defect on MRI, consistent with semicircular canal fibrosis following acute labyrinthine ischemia. Moreover, PSC fibrosis was related with poor functional outcome. We therefore suggest using balanced steady-state gradient-echo sequences a few weeks following an acute lesion of inner ear sensors to detect signal loss within membranous labyrinth consistent with post-ischemic fibrosis. Besides addressing the underlying etiology, signal loss might also offer clues on the functional behavior of the involved sensor over time. In cases of acute loss of inner ear function, a careful bedside examination supplemented by instrumental assessments, including vHIT and VEMPs, of vestibular receptors and afferents may be completed by MRI with balanced steady-state gradient-echo sequences at a later time to confirm the diagnosis and address both etiology and functional outcome

Re-energisation of AGN head-tail radio galaxies in the galaxy cluster ZwCl0634.1+47474

Low-frequency radio observations show an increasing number of radio galaxies located in galaxy clusters that display peculiar morphologies and spectral profiles. This is the result of the dynamical interaction of the galaxy with the surrounding medium. Studying this phenomenon is key to understanding the evolution of low-energy relativistic particles in the intracluster medium. We present a multi-frequency study of the three head-tail (HT) radio galaxies and the radio halo in the galaxy cluster ZwCl0634.1+4747. We make use of observations at four frequencies performed with LOFAR LBA (53 MHz), HBA (144 MHz), GMRT (323 MHz) and VLA (1518 MHz) data. The use of extremely low radio frequency observations, such as LOFAR at 53 and 144 MHz, allowed us to detect the extension of the tails up to a distance of ~ 1 Mpc. We extracted spectral profiles along the tails in order to identify possible departures from a pure ageing model, such as the Jaffe-Perola (JP) model, which only involves synchrotron and inverse-Compton losses. We found clear evidence of departures from this simple ageing model, such as surface brightness enhancement and spectral flattening along all of the tails. This can be interpreted as the consequence of particle re-acceleration along the tails. Possible explanations for this behaviour include the interaction between a shock and the radio tails or a turbulence-driven re-acceleration mechanism. We show that the latter scenario is able to reproduce the characteristic features that we observed in our profiles

A three-component giant radio halo: the puzzling case of the galaxy cluster Abell 2142

Turbulence introduced into the intra-cluster medium (ICM) through cluster merger events transfers energy to non-thermal components, and can trigger the formation of diffuse synchrotron radio sources. Typical diffuse sources in the forms of giant radio halos and mini-halos are found in merging and relaxed cool core galaxy clusters, respectively. On the other hand, recent observations have revealed an increasing complexity of the non-thermal phenomenology. Abell 2142 (A2142) is a mildly disturbed cluster that exhibits uncommon thermal and non-thermal properties. It is known to host a hybrid halo consisting of two components (H1 and H2), namely a mini-halo-like and an enigmatic elongated radio halo-like structure. We aim to investigate the properties, origin, and connections of each component. We present deep LOFAR observations of A2142 in the frequency ranges $30-78$ MHz and $120-168$ MHz. With complementary multi-frequency radio and X-ray data, we analyse the radio spectral properties of the halo and assess the connection between the non-thermal and thermal components of the ICM. We detected a third radio component (H3), which extends over the cluster volume on scales $\sim 2$ Mpc, embeds H1 and H2, and has a morphology that roughly follows the thermal ICM distribution. The radio spectral index is moderately steep in H1 ($\alpha=1.09\pm 0.02$) and H2 ($\alpha=1.15\pm 0.02$), but is steeper ($\alpha=1.57\pm 0.20$) in H3. The analysis of the thermal and non-thermal properties allowed us to discuss possible formation scenarios for each radio component. Turbulence from sloshing motions of low-entropy gas on different scales may be responsible for the origin of H1 and H2. We classified H3 as a giant ultra-steep spectrum radio halo, which could trace the residual activity from an old energetic merger and/or inefficient turbulent re-acceleration induced by ongoing minor mergers.Comment: 24 pages (including Appendix), 15 Figures (plus 4 Figures in Appendix), Accepted for publication by A&

Abell 746: A highly disturbed cluster undergoing multiple mergers

We present deep \textit{XMM-Newton}, Karl Jansky Very Large Array, and upgraded Giant Metrewave Radio Telescope observations of Abell 746, a cluster that hosts a plethora of diffuse emission sources that provide evidence for the acceleration of relativistic particles. Our new \textit{XMM-Newton} images reveal a complex morphology of the thermal gas with several substructures. We observe an asymmetric temperature distribution across the cluster: the southern regions exhibit higher temperatures, reaching $\sim$9\,keV, while the northern regions have lower temperatures ($\rm \leq4\,keV$), likely due to a complex merger. We find evidence of four surface brightness edges, of which three are merger-driven shock fronts. Combining our new data with the published LOw-Frequency ARray observations has unveiled the nature of diffuse sources in this system. The bright northwest relic shows thin filaments and high degree of polarization with aligned magnetic field vectors. We detect a density jump, aligned with the fainter relic to the north. To the south, we detect high-temperature regions, consistent with shock-heated regions and density jump coincident with the northern tip of the southern radio structure. Its integrated spectrum shows a high-frequency steepening. Lastly, we find that the cluster hosts large-scale radio halo emission. The comparison of the thermal and nonthermal emission reveals an anticorrelation between the bright radio and X-ray features at the center. Our findings suggest that Abell 746 is a complex system that involves multiple mergers.Comment: 21 pages, 13 figures, submitted to Ap

Structural basis for inhibition of homologous recombination by the RecX protein

The RecA/RAD51 nucleoprotein filament is central to the reaction of homologous recombination (HR). Filament activity must be tightly regulated in vivo as unrestrained HR can cause genomic instability. Our mechanistic understanding of HR is restricted by lack of structural information about the regulatory proteins that control filament activity. Here, we describe a structural and functional analysis of the HR inhibitor protein RecX and its mode of interaction with the RecA filament. RecX is a modular protein assembled of repeated three-helix motifs. The relative arrangement of the repeats generates an elongated and curved shape that is well suited for binding within the helical groove of the RecA filament. Structure-based mutagenesis confirms that conserved basic residues on the concave side of RecX are important for repression of RecA activity. Analysis of RecA filament dynamics in the presence of RecX shows that RecX actively promotes filament disassembly. Collectively, our data support a model in which RecX binding to the helical groove of the filament causes local dissociation of RecA protomers, leading to filament destabilisation and HR inhibition

A novel role for RecA under non-stress: promotion of swarming motility in Escherichia coli K-12

BACKGROUND: Bacterial motility is a crucial factor in the colonization of natural environments. Escherichia coli has two flagella-driven motility types: swimming and swarming. Swimming motility consists of individual cell movement in liquid medium or soft semisolid agar, whereas swarming is a coordinated cellular behaviour leading to a collective movement on semisolid surfaces. It is known that swimming motility can be influenced by several types of environmental stress. In nature, environmentally induced DNA damage (e.g. UV irradiation) is one of the most common types of stress. One of the key proteins involved in the response to DNA damage is RecA, a multifunctional protein required for maintaining genome integrity and the generation of genetic variation. RESULTS: The ability of E. coli cells to develop swarming migration on semisolid surfaces was suppressed in the absence of RecA. However, swimming motility was not affected. The swarming defect of a ΔrecA strain was fully complemented by a plasmid-borne recA gene. Although the ΔrecA cells grown on semisolidsurfaces exhibited flagellar production, they also presented impaired individual movement as well as a fully inactive collective swarming migration. Both the comparative analysis of gene expression profiles in wild-type and ΔrecA cells grown on a semisolid surface and the motility of lexA1 [Ind-] mutant cells demonstrated that the RecA effect on swarming does not require induction of the SOS response. By using a RecA-GFP fusion protein we were able to segregate the effect of RecA on swarming from its other functions. This protein fusion failed to regulate the induction of the SOS response, the recombinational DNA repair of UV-treated cells and the genetic recombination, however, it was efficient in rescuing the swarming motility defect of the ΔrecA mutant. The RecA-GFP protein retains a residual ssDNA-dependent ATPase activity but does not perform DNA strand exchange. CONCLUSION: The experimental evidence presented in this work supports a novel role for RecA: the promotion of swarming motility. The defective swarming migration of ΔrecA cells does not appear to be associated with defective flagellar production; rather, it seems to be associated with an abnormal flagellar propulsion function. Our results strongly suggest that the RecA effect on swarming motility does not require an extensive canonical RecA nucleofilament formation. RecA is the first reported cellular factor specifically affecting swarming but not swimming motility in E. coli. The integration of two apparently disconnected biologically important processes, such as the maintenance of genome integrity and motility in a unique protein, may have important evolutive consequences

Differential Requirements of Two recA Mutants for Constitutive SOS Expression in Escherichia coli K-12

Background Repairing DNA damage begins with its detection and is often followed by elicitation of a cellular response. In E. coli, RecA polymerizes on ssDNA produced after DNA damage and induces the SOS Response. The RecA-DNA filament is an allosteric effector of LexA auto-proteolysis. LexA is the repressor of the SOS Response. Not all RecA-DNA filaments, however, lead to an SOS Response. Certain recA mutants express the SOS Response (recAC) in the absence of external DNA damage in log phase cells. Methodology/Principal Findings Genetic analysis of two recAC mutants was used to determine the mechanism of constitutive SOS (SOSC) expression in a population of log phase cells using fluorescence of single cells carrying an SOS reporter system (sulAp-gfp). SOSC expression in recA4142 mutants was dependent on its initial level of transcription, recBCD, recFOR, recX, dinI, xthA and the type of medium in which the cells were grown. SOSC expression in recA730 mutants was affected by none of the mutations or conditions tested above. Conclusions/Significance It is concluded that not all recAC alleles cause SOSC expression by the same mechanism. It is hypothesized that RecA4142 is loaded on to a double-strand end of DNA and that the RecA filament is stabilized by the presence of DinI and destabilized by RecX. RecFOR regulate the activity of RecX to destabilize the RecA filament. RecA730 causes SOSC expression by binding to ssDNA in a mechanism yet to be determined