Manifesto for Digital Social Touch in Crisis

This qualitative exploratory research paper presents a Manifesto for Digital Social Touch in Crisis - a provocative call to action to designers, developers and researchers to rethink and reimagine social touch through a deeper engagement with the social and sensory aspects of touch. This call is motivated by concerns that social touch is in a crisis signaled by a decline in social touch over the past 2 decades, the problematics of inappropriate social touch, and the well documented impact of a lack of social touch on communication, relationships, and well-being and health. These concerns shape how social touch enters the digital realm and raise questions for how and when the complex space of social touch is mediated by technologies, as well the societal implications. The paper situates the manifesto in the key challenges facing haptic designers and developers identified through a series of interdisciplinary collaborative workshops with participants from computer science, design, engineering, HCI and social science from both within industry and academia, and the research literature on haptics. The features and purpose of the manifesto form are described, along with our rationale for its use, and the method of the manifesto development. The starting points, opportunities and challenges, dominant themes and tensions that shaped the manifesto statements are then elaborated on. The paper shows the potential of the manifesto form to bridge between HCI, computer science and engineers, and social scientists on the topic of social touch

Sustainable development and well-being: a philosophical challenge

This paper aims at gaining a better understanding of the inherent paradoxes within sustainability discourses by investigating its basic assumptions. Drawing on a study of the metaphoric references operative in moral language, we reveal the predominance of the 'well-being = wealth' construct, which may explain the dominance of the 'business case' cognitive frame in sustainability discourses (Hahn et al. in Acad Manag Rev 4015:18–42, 2015a). We incorporate economic well-being variables within a philosophical model of becoming well (Küpers in Cult Organ 11(3):221–231, 2005), highlighting the way in which these variables consistently articulate a combination of 'objective' and 'subjective' concerns. We then compare this broad understanding of well-being with the metaphors operative in the sustainable development discourse and argue that the sustainability discourse has fallen prey to an overemphasis on the 'business case'. We proceed to draw on Georges Bataille to challenge the predominance of these value priorities and to explore which mindshifts are required to develop a more comprehensive understanding of what is needed to enable 'sustainable development'

High- and low-flux acetate-free biofiltration: experimental assessment of calcium mass balance and intact parathyroid hormone behaviour.

We studied total calcium mass balance and plasma intact parathyroid hormone behaviour in 10 uraemic patients who underwent acetate-free biofiltration carried out in accordance with six different dialytic schedules, where either a polyacrylonitrile or a polysulphone membrane was used. Schedules 1 and 2 involved a reinfusion flow rate of 33.3 ml/min with a dialysate calcium concentration (DCa) of 1.75 and 2 mmol/l respectively; in schedule 3, 4, 5 and 6 reinfusion flow rate amounted to 50 ml/min and DCa was respectively of 1.75, 2, 2.25 and 2.5 mmol/l. Dehydration remained unchanged in all schedules: 700 g/h. Finally high- and low-flux acetate-free biofiltration are able to induce different Ca mass balance which may suit different therapeutic contexts. Ca mass balance was either positive or negative depending on reinfusion flow rate and DCa. With a reinfusion flow rate of 33.3 ml/min a DCa of at least 2 mmol/l was necessary to obtain a positive mass balance, while with a reinfusion flow rate of 50 ml/min DCa had to equal 2.25 mmol/l. In high-flux acetate-free biofiltration, the estimation of predialytic Ca2+ and DCa values, using a simple formula, allows prediction of the mass balance that will be attained. At the end of acetate-free biofiltration, intact parathyroid hormone always decreased when a polyacrylonitrile membrane was employed while it increased, in the presence of negative Ca mass balance with a polysulphone membrane

Headache is a risk factor for the onset of hypertension in pregnancy

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Endoscopic evaluation of gastrointestinal tract in patients with hereditary hemorrhagic telangiectasia and correlation with their genotypes.

Purpose:Hereditary hemorrhagic telangiectasia (HHT) is an autosomal-dominant vascular dysplasia characterized by telangiectases and arteriovenous malformations. Three causative genes are known: ENG (HHT-1), ACVRL1 (HHT-2), and SMAD4 (mutated in HHT in association with juvenile polyposis). Gastrointestinal bleeding is the most common symptom after epistaxis. The stomach and the duodenum are the main gastrointestinal sites of telangiectases. Our aim was to explore gastrointestinal tract of consecutive HHT patients to assess distribution, number, size, and type of telangiectases in relation to genotype.Methods:HHT patients underwent gastroduodenoscopy, video capsule endoscopy, and colonoscopy. Molecular analysis of ENG and ACVRL1 was performed to identify the disease-causing mutation.Results:Twenty-two patients (13 men; mean age: 59 ± 9 years) were analyzed: 7 with HHT-1, 13 with HHT-2, and 2 undefined. Gastrointestinal telangiectases were identified as follows: at gastroduodenoscopy in 86% of HHT-1 patients and in 77% of HHT-2 patients, at video capsule endoscopy in all HHT-1 patients and in 84% of HHT-2 patients, and at colonoscopy in 1 patient for each group. HHT-1 showed multiple telangiectases with a higher prevalence, more relevant in the duodenum.Conclusion:Our data demonstrate extensive involvement of the gastrointestinal tract with a more severe association in HHT-1. Gastroduodenoscopy provides significant information on gastrointestinal involvement, and video capsule endoscopy may be added in selected patients. Colonic polyps/adenomas were identified as occasional findings

Increase of circulating endothelial cells in patients with Hereditary Hemorrhagic Telangiectasia.

Hereditary Hemorrhagic Telangiectasia (HHT) is an autosomal dominant disorder characterized by vascular malformations. The genes known to be associated with HHT include ENG (HHT1), ACVRL1 (HHT2) and SMAD4 (JPHT). It has been reported that circulating CD34+ cell subsets repair damaged vessels. To investigate whether mobilization of these cells is present in the peripheral blood (PB) of HTT patients, we analyzed CD34+ cells, CD34+VEGFR-2+ progenitor or mature endothelial cells, and CD34+CD133+VEGFR-2- hematopoietic progenitor cells (HPCs). Cytofluorimetric analysis was performed in 150 HTT patients and 43 healthy subjects (CTRLs). In HTT patients, PB CD34+ cells were significantly increased; the frequency of endothelial cells was higher (P = 0.002), while the frequency of CD34+CD133+VEGFR-2- HPCs was lower (P = 0.00007) than in CTRLs. Results were comparable in patients with ENG or ACVRL1 gene mutation; in patients with ENG mutation, the frequency of the cell subsets inversely correlated with the age of the patients at time of sampling (CD34+), disease duration (CD34+VEGFR-2+), and age at disease onset (CD34+CD133+ VEGFR-2-). In conclusion, HHT patients show an increase of circulating endothelial cells and a decrease of HPCs. In patients with ENG mutation, the frequency of CD34+ endothelial cells correlates with specific clinical characteristics suggesting that their active turnover characterizes the initial phase of the disease

Pulmonary artery systolic pressure as estimated by TTE in a group of HHT patients.

Hereditary hemorrhagic telangiectasia (HHT) or Rendu syndrome-Osler-Weber disease, is an autosomal dominant vascular dysplasia characterized by epistaxis, mucocutaneous telangiectasias and arteriovenous malformations in specific locations mainly in liver, lungs and brain. The genes involved are two: ENG responsible for HHT1 and ACVRL1 associated with HHT2. We previously reported that estimated pulmonary artery systolic pressure (ePASP) was increased in a subgroup (9/68; 13,2%) of HHT patients in whom the clinical diagnosis defined according to Curaçao criteria was confirmed by the demonstration of mutations in ACVRL1 (Olivieri et al 2006). We extended our experience by performing Doppler transthoracic echocardiography (TTE) to estimate PASP in 104 patients (58 females), previously diagnosed with HHT according to Curaçao criteria. We found 79 ACVRL1 and 25 ENG mutations, and the distribution of the mutations in both genes resembles the general distribution in our lab. While no differences were observed for a ePASP in the whole group of HHT1/HHT2 patients, a trend for higher levels in HHT2 was observed when levels of a ePASP ≥40 mmHg were considered: HHT1 43,5±1,3.; 48,8±8,8 in HHT2. As expected a highly significant correlation was found between age and ePASP and, similarly, the presence of hepatic vascular malformations is significantly associated with the levels of ePASP in both HHT1/HHT2. Although not significant, the correlation between age and ePASP was slightly different in the two groups: the mean age of HHT1 showing values ≥40 mmHg was 72,2 while in HHT2 the mean age was 63,5

Efficacy of thalidomide in the treatment of severe recurrent epistaxis in hereditary hemorrhagic teleangiectasia: a comparison between HHT1 and 2.

Hereditary hemorrhagic telangiectasia (HHT: OMIM 187300 and 600376) is an autosomal dominant vascular dysplasia that affects 1 in 5-8000. The diagnosis is clinical and based on the presence of at least three of the “Curaçao criteria”: spontaneous and recurrent epistaxis, multiple telangiectases, visceral lesions (AVMs) in lungs, liver, brain; and finally a family history. Heterozygous mutations of activine receptor-like kinase-1 (ACVRL1) gene and endoglin (ENG) gene cause HHT2 and HHT1 respectively. Recurrent severe epistaxis is the most common presentation in HHT patients (95%), frequently leading to severe anemia requiring blood transfusions. Since angiogenesis has been implicated in the pathogenesis of HHT and since thalidomide has been shown to be a potent angiogenic inhibitor in experimental models, we tried to evaluate the effectiveness of thalidomide in reducing epistaxis and in the blood transfusions requirement. By assessing parameters such as: grading of epistaxis according to the severity score by Pagella et al (Acta Otolaryngol. 2013; 133(2):174-80), transfusion requirement and hemoglobin in the blood, we report results obtained on a group of 29 HHT patients treated with thalidomide for five months. We observed differences in the response to the use of thalidomide between HHT2 and HHT1 patients; in particular the first ones showed a reduction of transfusion requirement of 45,14% compared to HHT1 patients (5,77%). These data indicate a better response in patients with mutations in ACVRL1 and then you can think of to target treatment to patients preferentially HHT2. According to data in literature, thalidomide is metabolized in small part by CYP2C19, and since it is known that specific polymorphisms in these enzymes may modulate the activity of the drug, we set out to evaluate their presence in treated patients and how they can possibly modulate the answer and the side-effects of thalidomide. The results showed that the effects in patients (5) heterozygous for the polymorphism (*1/*2) have a lower reduction of epistaxis (37%) compared to wild type (46.49%)