VOX : furniture designed for public places

A trend in modern landscape architecture is to design pedestrian streets so that vehicles and people move in the same area. By doing this, traffic tends to slow down. On the market though, there is a lack of furniture that corresponds to the requirements of these kinds of public places. Therefore, I have designed this furniture, called VOX, which is planned to be used on streets, schoolyards and squares. One objective has been to promote the product to the industry. To achieve this, I have been in contact with people from different professions, which have all influenced my designprocess. For a time, I collaborated with the municipality of Uppsala who had great interests in my product. The development of VOX is presented as a design diary which includes early sketches, marketing and the making of a prototype. VOX is made in terrazzo concrete. I have obtained information about the material through books, interviews, Internet and by visiting concrete factories. One chapter in this booklet is a summary of my research and is unique in its kind since compiled publications about terrazzo concrete are rare. My hope is that this work can be used as a source for inspiration and knowledge, for students as well as for landscape architects in practice

Plasma levels of alpha1-antichymotrypsin and secretory leukocyte proteinase inhibitor in healthy and chronic obstructive pulmonary disease (COPD) subjects with and without severe α1-antitrypsin deficiency

BACKGROUND: Individuals with severe Z α1-antitrypsin (AAT) deficiency have a considerably increased risk of developing chronic obstructive lung disease (COPD). It has been hypothesized that compensatory increases in levels of other protease inhibitors mitigate the effects of this AAT deficiency. We analysed plasma levels of AAT, α1-antichymotrypsin (ACT) and secretory leukocyte protease inhibitor (SLPI) in healthy (asymptomatic) and COPD subjects with and without AAT deficiency. METHODS: Studied groups included: 71 asymptomatic AAT-deficient subjects (ZZ, n = 48 and SZ, n = 23, age 31 ± 0.5) identified during Swedish neonatal screening for AAT deficiency between 1972 and 1974; age-matched controls (MM, n = 57, age 30.7 ± 0.6); older asymptomatic ZZ (n = 10); healthy MM (n = 20, age 53 ± 9.6); and COPD patients (ZZ, n = 10, age 47.4 ± 11 and MM, n = 10, age 59.4 ± 6.7). Plasma levels of SLPI, AAT and ACT were analysed using ELISA and immunoelectrophoresis. RESULTS: No significant difference was found in plasma ACT and SLPI levels between the healthy MM and the ZZ or SZ subjects in the studied groups. Independent of the genetic variant, subjects with COPD (n = 19) had elevated plasma levels of SLPI and ACT relative to controls (n = 153) (49.5 ± 7.2 vs 40.7 ± 9.1 ng/ml, p < 0.001 and 0.52 ± 0.19 vs 0.40 ± 0.1 mg/ml, p < 0.05, respectively). CONCLUSION: Our findings show that plasma levels of ACT and SLPI are not elevated in subjects with genetic AAT deficiency compared MM controls and do not appear to compensate for the deficiency of plasma AAT

Chronic Intestinal Pseudo-Obstruction due to Buserelin-Induced Formation of Anti-GnRH Antibodies.

Background & Aims: A 30-year-old woman, treated with buserelin, an analogue of gonadotropin-releasing hormone (GnRH) (also called luteinizing hormone-releasing hormone, LH-RH), developed chronic intestinal pseudo-obstruction (CIPO). The sudden onset of this disease in a previously healthy woman perplexed us. CIPO refers to a gastrointestinal disorder that can have a variety of causes, such as drugs, among others. Thus, we wanted to examine whether in this patient the development of CIPO is related to the treatment with buserelin. Methods: The patient was examined using esophagogastroduodenoscopy, esophageal, and antroduodenojejunal manometry, gastric emptying tests, and histologic analyses and immunohistochemistry on full-thickness biopsies including staining with anti-GnRH antibody. Plasma samples were examined by the standard serologic analyses and specifically for the occurrence of anti-GnRH antibodies by enzyme-linked immunosorbent assay methods. Results: CIPO was diagnosed based on symptoms (abdominal pain, vomiting, and constipation), and the results of the clinical examinations, such as signs of esophageal aperistalsis, delayed gastric emptying, and small intestinal bursts. Histologic examination revealed a decreased number of myenteric neurons as well as increased neuronal degeneration and an abnormal immune profile. There was a loss of GnRH-containing neurons. The patient had high plasma titers of anti-GnRH antibodies, which occurred on the occasions of the treatment with buserelin. Conclusions: Our findings suggest that the patient has developed CIPO due to buserelin-induced formation of anti-GnRH antibodies destroying GnRH-producing neurons of the myenteric plexus

Increased plasma levels of serine proteinase inhibitors in lung cancer patients.

BACKGROUND: Tumor growth and invasiveness occur through infiltration of tumor cells into the host cells and by angiogenesis, which is modulated by proteinases and antiproteinases released from tumor cells that carry out tissue remodelling. A number of studies have revealed variations in the plasma levels of serine proteases and their inhibitors among tumor types. PATIENTS AND METHODS: By immunological methods we analysed the levels of serine protease inhibitors AAT, ACT and SLPI in newly diagnosed lung cancer patients (n=14) compared to non-smoker and smoker, age- and gender-matched control groups (n=16), and also in an expanded group of lung cancer patients with local tumors (n=14) and with metastasis (n=18). RESULTS: Our data show that plasma levels of AAT, ACT and SLPI were elevated in lung cancer patients by 1.43-fold, p<0.01, 2.57-fold, p<0.01 and 1.6-fold, p<0.001, respectively when compared to controls. In addition, we found that levels of AAT and ACT were higher by 1.47-fold, p<0.001 and 2.27-fold, p<0.001, respectively in lung cancer cases with metastasis compared to localized tumor. CONCLUSION: These inhibitor levels may provide measures of cancer progression in individual patients and possibly offer useful information for an understanding of the mechanisms of metastasis

Secreted leukocyte protease inhibitor is present in aqueous humours from cataracts and other eye pathologies.

Previous studies identified serine, cysteine and metalloproteases in normal aqueous humours (AH) and suggested that a balance between proteases and their inhibitors may play a role in the modulation of the AH outflow. We aimed to determine whether secretory leukocyte protease inhibitor (SLPI), a serine protease inhibitor, is present in AH of patients with cataract and other eye pathologies. AH was collected from 117 cataract patients of which 55 were diagnosed with more when one eye disease: cataract only (n = 62), pseudoexfoliation (PEX) (n = 26), glaucoma (n = 6), diabetes retinopathy (n = 4), iritis-uveitis (n = 4) and macular degeneration (n = 28). The total protein in AH was determined by a Bradford assay and SLPI was analyzed by Western blot and ELISA methods. The average concentration of total protein and SLPI in AH samples was 160 +/- 15 mu g/ml (n = 117, +/- SEM) and 500 +/- 94 pg/ml (n = 105), respectively. The cataract patients with additional eye disease(s) showed higher protein levels (201 + 35 mu g/ml) than cataract (controls) (128 31 pg/ml), P < 0.01. It is noteworthy that no correlation was found between SLPI and the total protein concentrations in AH, but SLPI was positively correlated with age (r = 0.2, P < 0.05). No statistical difference in SLPI levels was found between controls (cataract) and other pathologies, while patients with iritis/uveitis had higher SLPI levels compared to those with diabetes (P < 0.05). We show here for the first time that SLPI is present in AH and may play a role as well as serve as a marker in pathological states. (c) 2005 Elsevier Ltd. All rights reserved

Mutations in the low-density lipoprotein receptor gene in Swedish familial hypercholesterolaemia patients: clinical expression and treatment response

BACKGROUND: Familial hypercholesterolaemia, an autosomal co-dominant disorder caused by defects in the low-density lipoprotein receptor gene, is strongly associated with premature development of cardiovascular disease. METHODS: In this study, we have applied a gene screening method in a population of familial hypercholesterolaemia patients in order to describe the genetic background of the disease in southern Sweden. These patients were studied with the aim of relating the presence of the different mutations to the clinical expression of the disease and to the response to pharmacological treatment. RESULTS: In 16 out of 21 patients, potentially disease-causing low-density lipoprotein receptor gene defects were found, including five not previously described alterations (C240-->F, C122-->stop, C356-->Y, 785insG, 165delG). No defects in apolipoprotein B were found. One group of patients (n = 4) carried the mutation C122-->stop and another group of patients (n = 4) a mutation causing the substitution W66-->G. Patients in the two genotype subgroups were very similar with respect to lipid levels before treatment. CONCLUSION: A tendency towards differential susceptibility to treatment with statins was observed for the patient groups, encouraging further comparative studies of heterozygous FH patients