Emotietheorieën

Emotietheorieën zien veelal cognitieve of non-cognitieve elementen als essentieel voor emoties. In dit essay wordt, door een commentaar op William James en Jesse Prinz, beargumenteerd dat een theorie over emoties zowel cognitieve als non-cognitieve elementen moet bevatten. Daarnaast wordt aangetoond dat een dergelijke theorie compatibel is met empirisch onderzoek op het gebied van emotie

Treatment of the Guillain-Barré syndrome

The Guillain-Barre syndrome (GBS) is an inflammatory polyneuropathy with an incidence of 1-1.8/100,000. It is characterised by an acute or subacute onset and a progressive phase of less than four weeks, followed by a plateau phase of variable duration [106, 111]. Improvement then starts spontaneously; about 80% of the patients revover completely [135]. During the disease, 10-23% of the patients require artificial ventilation and there is still a mortality of 3-5%. Ultimately, 10-22% of the patients remain disabled [106, 113, 135]. Since not all patients make an uneventful, complete recovery, the search for an effective treatment is going on continuously. The possible role of humoral components in the pathogenesis of GBS [30] prompted an open study with plasma exchange (PE) in a single patient with severe GBS. That was very successful [14]. After numerous case reports [28, 58, 109, 130, 141, 149, 172] and several clinical trials [50, 57, 61, 131] examining the effects of PE in GBS patients, PE is now generally accepted as a treatment for patients with severe GBS [26]. PE carries, however, certain risks [69, 159]. It is a cumbersome procedure and therefore not widely applicable. This prompted us to investigate an alternative treatment with immunoglobulins, given intravenously (Igiv), which forms the basis for this thesis. The aim of this study was to investigate a new, and relatively simple treatment for patients with Guillain-Barre syndrome (GBS)

Methodologies to increase public transport mode share in Sydney and Perth

University of Technology, Sydney. Faculty of Engineering and Information Technology.This Masters’ Thesis has evolved as an iterative learning process driven initially by the compilation and understanding of transportation usage data. The research phase began with a clear goal to understand the historical context of transportation modal share. The initial objective and scope of the research was therefore to collate as much data as possible to deliver an understanding of the recent trends in Sydney and Perth. This data built on the “Transportation / Land Use Cycle” theories which were evident in my Capstone Project work. The scope of the data collection was to discover statistically significant trends such as links between:- • Accessibility to the CBD and trip generation; • Accessibility to transportation options (socio-economic status and urban location) and its impact on public transport usage; • Whether the purpose of the trip had an impact on the mode chosen; and • Whether household composition and dwelling densities had an impact on motor vehicle usage

Guillain-Barré syndrome: a century of progress

In 1916, Guillain, Barré and Strohl reported on two cases of acute flaccid paralysis with high cerebrospinal fluid protein levels and normal cell counts — novel findings that identified the disease we now know as Guillain–Barré syndrome (GBS). 100 years on, we have made great progress with the clinical and pathological characterization of GBS. Early clinicopathological and animal studies indicated that GBS was an immune-mediated demyelinating disorder, and that severe GBS could result in secondary axonal injury; the current treatments of plasma exchange and intravenous immunoglobulin, which were developed in the 1980s, are based on this premise. Subsequent work has, however, shown that primary axonal injury can be the underlying disease. The association of Campylobacter jejuni strains has led to confirmation that anti-ganglioside antibodies are pathogenic and that axonal GBS involves an antibody and complement-mediated disruption of nodes of Ranvier, neuromuscular junctions and other neuronal and glial membranes. Now, ongoing clinical trials of the complement inhibitor eculizumab are the first targeted immunotherapy in GBS

Increased Circulating T Cell Reactivity to GM1 Ganglioside in Patients with Guillain-Barre Syndrome

This study was performed to determine whether increased ganglioside-specific T cell reactivity can be detected in the peripheral blood of patients with Guillain-Barre syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). T cell responsiveness to the gangliosides GM1, GM3, GD1a, GD1b, GD3, GT1b, GQ1b and sulphatide was assessed in peripheral blood mononuclear cells from untreated GBS patients (57), CIDP patients (43), patients with other peripheral neuropathies (55) and healthy control subjects (74) in a standard 6-day proliferation assay. Increased T cell reactivity to GM1 occurred in GBS patients compared to healthy controls and patients with other neuropathies. There was increased reactivity to GM3 in GBS patients compared to patients with other neuropathies but not compared to healthy controls. The frequencies of increased T cell reactivity to GM1 and GM3 in CIDP patients were intermediate between those of GBS patients and controls. We suggest that T cell reactivity to gangliosides might play a contributory role in the pathogenesis of GBS and perhaps CIDP

Совершенствование механизмов формирования доходов бюджета АРК

Целью нашей работы является исследование механизмов формирования доходов бюджета Автономной Республики Крым и разработка мероприятий по их совершенствованию

Soluble Beta-Amyloid Precursor Protein Is Related to Disease Progression in Amyotrophic Lateral Sclerosis

Background: Biomarkers of disease progression in amyotrophic lateral sclerosis (ALS) could support the identification of beneficial drugs in clinical trials. We aimed to test whether soluble fragments of beta-amyloid precursor protein (sAPPa and sAPPß) correlated with clinical subtypes of ALS and were of prognostic value. Methodology/Principal Findings: In a cross-sectional study including patients with ALS (N = 68) with clinical follow-up data over 6 months, Parkinson’s disease (PD, N = 20), and age-matched controls (N = 40), cerebrospinal fluid (CSF) levels of sAPPa a, sAPPß and neurofilaments (NfH SMI35) were measured by multiplex assay, Progranulin by ELISA. CSF sAPPa and sAPPß levels were lower in ALS with a rapidly-progressive disease course (p = 0.03, and p = 0.02) and with longer disease duration (p = 0.01 and p = 0.01, respectively). CSF NfH SMI35 was elevated in ALS compared to PD and controls, with highest concentrations found in patients with rapid disease progression (p,0.01). High CSF NfH SMI3 was linked to low CSF sAPPa and sAPPß (p = 0.001, and p = 0.007, respectively). The ratios CSF NfH SMI35 /CSF sAPPa,-ß were elevated in patients with fast progression of disease (p = 0.002 each). CSF Progranulin decreased with ongoing disease (p = 0.04). Conclusions: This study provides new CSF candidate markers associated with progression of disease in ALS. The data suggest that a deficiency of cellular neuroprotective mechanisms (decrease of sAPP) is linked to progressive neuro-axona

Patients Enrolled in Large Randomized Clinical Trials of Antiplatelet Treatment for Prevention After Transient Ischemic Attack or Ischemic Stroke Are Not Representative of Patients in Clinical Practice: the Netherlands Stroke Survey

Background and Purpose—Many randomized clinical trials have evaluated the benefit of long-term use of antiplatelet drugs in reducing the risk of new vascular events in patients with a recent transient ischemic attack or ischemic stroke. Evidence from these trials forms the basis for national and international guidelines for the management of nearly all such patients in clinical practice. However, abundant and strict enrollment criteria may limit the validity and the applicability of results of randomized clinical trials to clinical practice. We estimated the eligibility for participation in landmark trials of antiplatelet drugs of an unselected group of patients with stroke or transient ischemic attack from a national stroke survey. Methods—Nine hundred seventy-two patients with transient ischemic at

Intensive care unit—acquired weakness (ICUAW) and muscle wasting in critically ill patients with severe sepsis and septic shock

Sepsis presents a major health care problem and remains one of the leading causes of death within the intensive care unit (ICU). Therapeutic approaches against severe sepsis and septic shock focus on early identification. Adequate source control, administration of antibiotics, preload optimization by fluid resuscitation and further hemodynamic stabilisation using vasopressors whenever appropriate are considered pivotal within the early—golden—hours of sepsis. However, organ dysfunction develops frequently in and represents a significant comorbidity of sepsis. A considerable amount of patients with sepsis will show signs of severe muscle wasting and/or ICU-acquired weakness (ICUAW), which describes a frequently observed complication in critically ill patients and refers to clinically weak ICU patients in whom there is no plausible aetiology other than critical illness. Some authors consider ICUAW as neuromuscular organ failure, caused by dysfunction of the motor unit, which consists of peripheral nerve, neuromuscular junction and skeletal muscle fibre. Electrophysiologic and/or biopsy studies facilitate further subclassification of ICUAW as critical illness myopathy, critical illness polyneuropathy or critical illness myoneuropathy, their combination. ICUAW may protract weaning from mechanical ventilation and impede rehabilitation measures, resulting in increased morbidity and mortality. This review provides an insight on the available literature on sepsis-mediated muscle wasting, ICUAW and their potential pathomechanisms