multiphysics numerical investigation on the aeroelastic stability of a le mans prototype car

Abstract In the analysis and design of racing competition cars, numerical tools allow to investigate a wide range of solutions in short time and with high confidence in results. The great available computational power permits to combine simulation software so that different physics involved can be tackled at the same time. An important class of multi-physics simulations for motor sport addresses the fluid-structure interactions happening between the aerodynamic components of the car and the surrounding flow: this interaction can induce structural deformations and vibrations which, in turn, can influence the surrounding fluxes. In this paper, the flutter analysis of the front wing splitter mounted on the 2001 Le Mans Prototype car by Dallara (LMP1) is presented. The study was set up adopting high fidelity CAE models: a 400k shell elements FEM represents the full front wing assembly including the mounting frame, a 240M cells CFD represents the full car immersed in a box shaped wind tunnel. FEM extracted structural modal shapes are mapped onto the CFD mesh adopting Radial Basis Functions (RBF) mesh morphing so that the surfaces of the CFD model can be deformed according to retained modes. Such deformation is then propagated so that the volume mesh is adapted accordingly. The elastic CFD model with modes embedded was then loaded by applying a transient signal individually to each retained mode with a smoothed step function. A Reduced Order Model (ROM) for the aerodynamics of the coupled system was then extracted combining the results of the individual transient run. The critical speed experimentally observed to be in the operating range of the car was captured by the model quite well. The same workflow was then adopted to investigate a different design in which a stiffener has been introduced to increase the first mode natural frequency from 40Hz to 49.4Hz. Flutter speed was increased and moved outside the vehicle range. The car equipped with the improved part proved to perform on the track without previously detected instabilities

The clinical phenotype of autosomal dominant lateral temporal lobe epilepsy related to reelin mutations

Objective To describe the clinical phenotype of 7 families with Autosomal Dominant Lateral Temporal Lobe Epilepsy (ADLTE) related to Reelin (RELN) mutations comparing the data with those observed in 12 LGI1-mutated pedigrees belonging to our series. Methods Out of 40 Italian families with ADLTE, collected by epileptologists participating in a collaborative study of the Commission for Genetics of the Italian League against Epilepsy encompassing a 14-year period (2000\u20132014), 7 (17.5%) were found to harbor heterozygous RELN mutations. The whole series also included 12 (30%) LGI1 mutated families and 21 (52.5%) non-mutated pedigrees. The clinical, neurophysiological, and neuroradiological findings of RELN and LGI1 mutated families were analyzed. Results Out of 28 affected individuals belonging to 7 RELN mutated families, 24 had sufficient clinical data available for the study. In these patients, the epilepsy onset occurred at a mean age of 20 years, with focal seizures characterized by auditory auras in about 71% of the cases, associated in one-third of patients with aphasia, visual disturbances or other less common symptoms (vertigo or d\ue9j\ue0-vu). Tonic\u2013clonic seizures were reported by almost all patients (88%), preceded by typical aura in 67% of cases. Seizures were precipitated by environmental noises in 8% of patients and were completely or almost completely controlled by antiepileptic treatment in the vast majority of cases (96%). The interictal EEG recordings showed epileptiform abnormalities or focal slow waves in 80% of patients, localized over the temporal regions, with marked left predominance and conventional 1,5T MRI scans were not contributory. By comparing these findings with those observed in families with LGI1 mutations, we did not observe significant differences except for a higher rate of left-sided EEG abnormalities in the RELN group. Significance Heterozygous RELN mutations cause a typical ADLTE syndrome, indistinguishable from that associated with LGI1 mutations

Treatment strategy for vertebral metastases from anal squamous cell carcinoma: a comprehensive literature review and case report

Purpose/aim of the study: Purpose/aim of the study:Central nervous system (CNS), skull, and vertebral metastases from anal squamous cell carcinoma (SCC) are an exceedingly rare entity. We report the first case of multiple vertebral metastases from a primary anal SCC with the aim of define a target therapeutic strategy.Case presentation: We present the case of a 68-year-old male admitted to our hospital for acute exacerbation chronic low back pain and left L2 radiculopathy. His medical history included the diagnosis of a human papilloma virus related, moderately differentiated anal SCC (cT3N0M0-stage IIB), treated with standard chemoradiotherapy regimen two years earlier. Spinal magnetic resonance imaging revealed an isolated solid lesion of the L2 vertebral body. After the surgical removal, histopathological examination confirmed the diagnosis of moderately differentiated SCC. At 1-month radiological follow-up, two new lesions at the level of T7 to T11 were identified. Additional chemotherapy and radiotherapy for metastatic localization of L2, T7, and T11 were administered. Two-year follow-up demonstrated a radiologically and clinically well-controlled disease. To supplement our case, a systematic literature review on the CNS, skull, and vertebral metastases and their treatments has been performed.Conclusion: Despite several proposed guidelines for the management of vertebral metastases, at present, a universally accepted treatment strategy for vertebral metastases from anal SCC has not been defined. Based on our clinical experience and literature review, in case of vertebral metastases from anal SCC, a prompt and aggressive, local and systemic, and multimodal treatment of the vertebral lesions may be paramount to improve the patient outcomes

Developmental venous anomaly associated with dural arteriovenous fistula: Etiopathogenesis and hemorrhagic risk

Introduction: Developmental venous anomalies (DVAs) have traditionally been defined as non-pathological congenital lesions. Compared to isolated DVAs, the association of DVAs with arteriovenous shunts seems to have a more adverse clinical connotation. In this review, we describe the association between DVA and dAVF and discuss the hemorrhagic risk. We also advance a hypothesis about the potential de novo formation of a DVA and challenge the dogma about their “developmental” or “congenital” nature. Methods: A systematic review of the literature on the association of DVA and dAVF was performed in accordance with the PRISMA-P (Preferred Reporting Items for Systematic Review and Meta-Analysis Protocols) guidelines. Results: A number of 678 papers was initially identified, but only 9 studies were included in the final qualitative analysis. Most of the patients presented with bleeding (56%), with a median GCS of 14 (range 10–15). In 56% of the cases the DVA had a supratentorial location. Supratentorial DVAs mostly drained in the superior sagittal sinus (80%), while all of infratentorial/combined DVAs drained in deep ependymal veins of the 4th ventricle. All the supratentorial dAVFs drained into the superior sagittal sinus, while the infratentorial/combined dAVFs mostly drained in the jugular bulb, Vein of Rosenthal, or transverse-sigmoid sinuses (75%). Most of the dAVFs were classified as Cognard type IIa + b (67%), while in a smaller number of cases type I (22%) and type V (11%). The dAVF was the target of treatment in each case and most patients underwent endovascular treatment (78%). The dAVF was completely occluded in 78% of cases and no periprocedural complications were reported. Conclusion: The clinical presentation, radiological findings, and treatment outcomes of DVAs and associated dAVFs have been discussed. Despite the general opinion that DVAs are benign congenital lesions, increasing epidemiological and radiological evidence supports a potential acquired origin, and the venous system seem to play a pivotal role in their post-natal genesis and development

Propofol 1% and propofol 2% are equally effective and well tolerated during anaesthesia of patients undergoing elective craniotomy for neurosurgical procedures

BACKGROUND: The 2% formulation of the intravenous anaesthetic agent, propofol (Diprivan), delivers half the amount of lipid compared with the original 1% formulation. This may provide an acceptable alternative for patients who have an impaired ability to metabolise lipids. METHODS: This study was a multicentre, randomised, open comparison of parallel groups. Seventy-three adult patients undergoing elective craniotomy in neurosurgery were randomised to receive either propofol 1% (10 mg/ml) or propofol 2% (20 mg/ml) for induction and maintenance of anaesthesia. RESULTS: Analysis of induction time (199 s, 1%; 202 s, 2%; p > 0.05) and induction dose (1.13 mg/kg, 1.12 mg/kg; p > 0.05) shows that propofol 1% and propofol 2% are pharmacodynamically equivalent. Both formulations were similar regarding overall administration rates, recovery times, haemodynamic variables and tolerability. Plasma triglyceride levels, were lower in the propofol 2% group compared with the propofol 1% group, and significantly lower (p < 0.05) from 1 to 4 hours after induction. CONCLUSIONS: We conclude that propofol 2% is as effective and as well-tolerated as propofol 1% for anaesthesia and is an acceptable alternative to propofol 1% in patients undergoing elective craniotomy in neurosurgery. The lower lipid load suggests it may be of particular benefit to patients with disorders of lipid metabolism

Microsurgical transcranial approaches to the posterior surface of petrosal portion of the temporal bone: quantitative analysis of surgical volumes and exposed areas

Different microsurgical transcranial approaches (MTAs) have been described to expose the posterior surface of the petrous bone (PPB). A quantitative, anatomical comparison of the most used MTAs, for specific areas of the PPB, is not available. Anatomical dissections were performed on five formalin-fixed, latex-injected cadaver heads (10 sides). Six MTAs were analyzed: Kawase approach (KWA), retrosigmoid approach (RSA), retrosigmoid approach with suprameatal extension (RSAS), retrolabyrinthine approach (RLA), translabyrinthine approach (TLA), and transcochlear approach (TCA). Surgical volumes and exposed areas of each approach were quantified with a dedicated neuronavigation system (ApproachViewer, part of GTx-Eyes II, University Health Network, Toronto, Canada) and adjuvant software (ITK-SNAP and Autodesk Meshmixer 3.5). Areas and volumes were compared using linear mixed models. TCA provided the best exposure of Trautmann’s triangle and the retromeatal, suprameatal, meatal, and premeatal regions. RSAs provided the best exposure of the inframeatal region, with RSAS gaining significant exposure of the suprameatal region. KWA had the highest surgical volume, and RLA the lowest. Transpetrosal approaches offer the widest exposure of PPB proportionally to their invasiveness. Retrosigmoid approaches, which get to the studied region through a postero-lateral path, are paramount for the exposure of the inframeatal and suprameatal region and, given the adequate exposure of the remaining PPB, represent an effective approach for the cerebellopontine angle (CPA). These anatomical findings must be considered with approach-related morbidity and the pathological features in order to choose the most appropriate approach in clinical practice

A Nutritional Formula Enriched With Arginine, Zinc, and Antioxidants for the Healing of Pressure Ulcers

BACKGROUND: Trials on specific nutritional supplements for the treatment of pressure ulcers (PUs) have been small, inconsistent in their formulations, or unsuccessful in controlling for total supplement calorie or protein content. OBJECTIVE: To evaluate whether supplementation with arginine, zinc, and antioxidants within a high-calorie, high-protein formula improves PU healing. DESIGN: Multicenter, randomized, controlled, blinded trial. (ClinicalTrials.gov: NCT01107197). SETTING: Long-term care and home care services. PATIENTS: 200 adult malnourished patients with stage II, III, and IV PUs. INTERVENTIONS: An energy-dense, protein-rich oral formula enriched with arginine, zinc, and antioxidants (400 mL/d) or an equal volume of an isocaloric, isonitrogenous formula for 8 weeks. MEASUREMENTS: The primary end point was the percentage of change in PU area at 8 weeks. Secondary end points included complete healing, reduction in the PU area of 40% or greater, incidence of wound infections, the total number of dressings at 8 weeks, and the percentage of change in area at 4 weeks. RESULTS: Supplementation with the enriched formula (n = 101) resulted in a greater reduction in PU area (mean reduction, 60.9% [95% CI, 54.3% to 67.5%]) than with the control formula (n = 99) (45.2% [CI, 38.4% to 52.0%]) (adjusted mean difference, 18.7% [CI, 5.7% to 31.8%]; P = 0.017). A more frequent reduction in area of 40% or greater at 8 weeks was also seen (odds ratio, 1.98 [CI, 1.12 to 3.48]; P = 0.018). No difference was found in terms of the other secondary end points. LIMITATION: Participation was restricted to patients who were malnourished, were able to drink oral supplements, and were living in long-term care institutions or receiving home care services. CONCLUSION: Among malnourished patients with PU, 8 weeks of supplementation with an oral nutritional formula enriched with arginine, zinc, and antioxidants improved PU healing

Heterozygous reelin mutations cause autosomal-dominant lateral temporal epilepsy

Autosomal-dominant lateral temporal epilepsy (ADLTE) is a genetic epilepsy syndrome clinically characterized by focal seizures with prominent auditory symptoms. ADLTE is genetically heterogeneous, and mutations in LGI1 account for fewer than 50% of affected families. Here, we report the identification of causal mutations in reelin (RELN) in seven ADLTE-affected families without LGI1 mutations. We initially investigated 13 ADLTE-affected families by performing SNP-array linkage analysis and whole-exome sequencing and identified three heterozygous missense mutations co-segregating with the syndrome. Subsequent analysis of 15 small ADLTE-affected families revealed four additional missense mutations. 3D modeling predicted that all mutations have structural effects on protein-domain folding. Overall, RELN mutations occurred in 7/40 (17.5%) ADLTE-affected families. RELN encodes a secreted protein, Reelin, which has important functions in both the developing and adult brain and is also found in the blood serum. We show that ADLTE-related mutations significantly decrease serum levels of Reelin, suggesting an inhibitory effect of mutations on protein secretion. We also show that Reelin and LGI1 co-localize in a subset of rat brain neurons, supporting an involvement of both proteins in a common molecular pathway underlying ADLTE. Homozygous RELN mutations are known to cause lissencephaly with cerebellar hypoplasia. Our findings extend the spectrum of neurological disorders associated with RELN mutations and establish a link between RELN and LGI1, which play key regulatory roles in both the developing and adult brain