Numerical and asymptotic solutions of generalised Burgers’ equation

The generalised Burgers’ equation has been subject to a considerable amount of research on how the equation should behave according to asymptotic analysis, however there has been limited research verifying the asymptotic analysis. In order to verify the asymptotic analysis, this paper aims to run long time and detailed numerical simulations of Burgers’ equation by employing suitable rescalings of Burgers’ equation. It is hoped that this technique will make it possible to notice subtle changes in the shock structure which would otherwise be impossible to observe. The main aim of this paper is to validate the numerical methods used in order to allow further research into shock evolution where further relaxation effects will be included

Cervical collar or physiotherapy versus wait and see policy for recent onset cervical radiculopathy: randomised trial

Objective To evaluate the effectiveness of treatment with collar or physiotherapy compared with a wait and see policy in recent onset cervical radiculopathy

Automatic detection of actionable findings and communication mentions in radiology reports using natural language processing

__Objectives:__ To develop and validate classifiers for automatic detection of actionable findings and documentation of nonroutine communication in routinely delivered radiology reports. __Me

Assessment of actionable findings in radiology reports

Purpose: The American College of Radiology (ACR) Actionable Reporting Work Group defined three categories of imaging findings that require additional, nonroutine communication wit

PMP22 related neuropathies: Charcot-Marie-Tooth disease type 1A and Hereditary Neuropathy with liability to Pressure Palsies

PMP22 related neuropathies comprise (1) PMP22 duplications leading to Charcot-Marie-Tooth disease type 1A (CMT1A), (2) PMP22 deletions, leading to Hereditary Neuropathy with liability to Pressure Palsies (HNPP), and (3) PMP22 point mutations, causing both phenotypes. Overall prevalence of CMT is usually reported as 1:2,500, epidemiological studies show that 20-64% of CMT patients carry the PMP22 duplication. The prevalence of HNPP is not well known. CMT1A usually presents in the first two decades with difficulty walking or running. Distal symmetrical muscle weakness and wasting and sensory loss is present, legs more frequently and more severely affected than arms. HNPP typically leads to episodic, painless, recurrent, focal motor and sensory peripheral neuropathy, preceded by minor compression on the affected nerve. Electrophysiological evaluation is needed to determine whether the polyneuropathy is demyelinating. Sonography of the nerves can be useful. Diagnosis is confirmed by finding respectively a PMP22 duplication, deletion or point mutation. Differential diagnosis includes other inherited neuropathies, and acquired polyneuropathies. The mode of inheritance is autosomal dominant and de novo mutations occur. Offspring of patients have a chance of 50% to inherit the mutation from their affected parent. Prenatal testing is possible; requests for prenatal testing are not common. Treatment is currently symptomatic and may include management by a rehabilitation physician, physiotherapist, occupational therapist and orthopaedic surgeon. Adult CMT1A patients show slow clinical progression of disease, which seems to reflect a process of normal ageing. Life expectancy is norma

The frontotemporal syndrome of ALS is associated with poor survival

Thirty percent of ALS patients have a frontotemporal syndrome (FS), defined as behavioral changes or cognitive impairment. Despite previous studies, there are no firm conclusions on the effect of the FS on survival and the use of non-invasive ventilation (NIV) in ALS. We examined the effect of the FS on survival and the start and duration of NIV in ALS. Behavioral changes were defined as >22 points on the ALS-Frontotemporal-Dementia-Questionnaire or ≥3 points on ≥2 items of the Neuropsychiatric Inventory. Cognitive impairment was defined as below the fifth percentile on ≥2 tests of executive function, memory or language. Classic ALS was defined as ALS without the frontotemporal syndrome. We performed survival analyses from symptom ons

Differential diagnosis in spinal and bulbar muscular atrophy clinical and molecular aspects

Kennedy disease is caused by an enlarged trinucleotide repeat sequence within the androgen receptor gene. We report here seven male patients with a benign motor neuron syndrome highly analogous to Kennedy disease but with a normal trinucleotide repeat