Modernity from Far East. Kazuo Shinohara’s Fourth Space

This paper is funded by the School of Doctorate Studies of the University Iuav of Venice and will be part of my PhD dissertation about Kazuo Shinohara’s work. Since the Japanese book Jutaku kenchiku (Residential Architecture) by Kazuo Shinohara has never been translated into English, the quotations reported here have been translated by me, thanks to Mr Yosuke Taki who did the Italian translation for me.Since, according to Kenneth Frampton, 'regional or national cultures must today, more than ever, be ultimately constituted as locally inflected manifestations of “world culture”’, contemporary Japanese culture would be in this sense the 'world culture' par excellence, structured on two important cultural imports - the first occurred between the 6th and 7th centuries when from China was introduced the ideographic writing, Confucian model of society and along with them Indian Buddhism; and the second one, during the late 19th century, when for the rapid modernization of the country Western politics, science and technology were adopted. Having soon faced, and deeply questioned, the possibilities and problems of a global dimension of the thought, Japanese culture could be considered an original synthesis of universality and local identity where, although the many contradictions, the meeting with the stranger allowed to discover what ‘not to be’, rather than what to be. Starting from the other side of modernity, and tracing the different aspects of the adoption of Modern Movement in Japan, aim of this paper is to introduce the figure of the Japanese architect Kazuo Shinohara (1925-2006) who unveiled the plurality and richness of our spatial structures, the universal and the particular in which we are immersed, most of the time, without consciousness.info:eu-repo/semantics/publishedVersio

KAP1 is a Novel Substrate for the Arginine Methyltransferase PRMT5

KRAB-associated protein 1 (KAP1), the transcriptional corepressor of Kruppel-associated box zinc finger proteins (KRAB-ZFPs), is subjected to multiple post-translational modifications that are involved in fine-tuning of the multiple biological functions of KAP1. In previous papers, we analyzed the KAP1-dependent molecular mechanism of transcriptional repression mediated by ZNF224, a member of the KRAB-ZFP family, and identified the protein arginine methyltransferase PRMT5 as a component of the ZNF224 repression complex. We demonstrated that PRMT5-mediated histone arginine methylation is required to elicit ZNF224 transcriptional repression. In this study, we show that KAP1 interacts with PRMT5 and is a novel substrate for PRMT5 methylation. Also, we present evidence that the methylation of KAP1 arginine residues regulate the KAP1-ZNF224 interaction, thus suggesting that this KAP1 post-translational modification could actively contribute to the regulation of ZNF224-mediated repression

Learning from participatory practices : the integrated management plan for Petra World Heritage Site in Jordan

When the Petra World Heritage Site Integrated Management Plan was officially endorsed in 2019, it was the first management plan for the site to be legally recognised. The plan also uniquely emerged from a sophisticated interactive and participatory process designed to engage with as many stakeholders as possible to build consensus and foster interdisciplinary approaches to long-standing issues. Over a two-year period, from inception and planning to the final endorsement of the Integrated Management Plan, a dedicated technical team facilitated collaborative work practices and enabled the co-creation of management policies. This paper is a reflexive evaluation of the process by the team and draws on first-hand accounts and experiences to evaluate the impacts this methodology and approach has had on stakeholders and its longer-term legacies. Although Petra is a complex site facing significant pressures and multifaceted user demands, the participatory process has nonetheless empowered stakeholders who had not traditionally engaged in decision-making processes to become more engaged and established a management planning approach that can be adapted for cultural heritage sites in Jordan and in the wider region

Hematopoietic Cell Transplantation Cures Adenosine Deaminase 2 Deficiency: Report on 30 Patients

PURPOSE: Deficiency of adenosine deaminase 2 (DADA2) is an inherited inborn error of immunity, characterized by autoinflammation (recurrent fever), vasculopathy (livedo racemosa, polyarteritis nodosa, lacunar ischemic strokes, and intracranial hemorrhages), immunodeficiency, lymphoproliferation, immune cytopenias, and bone marrow failure (BMF). Tumor necrosis factor (TNF-α) blockade is the treatment of choice for the vasculopathy, but often fails to reverse refractory cytopenia. We aimed to study the outcome of hematopoietic cell transplantation (HCT) in patients with DADA2. METHODS: We conducted a retrospective study on the outcome of HCT in patients with DADA2. The primary outcome was overall survival (OS). RESULTS: Thirty DADA2 patients from 12 countries received a total of 38 HCTs. The indications for HCT were BMF, immune cytopenia, malignancy, or immunodeficiency. Median age at HCT was 9 years (range: 2-28 years). The conditioning regimens for the final transplants were myeloablative (n = 20), reduced intensity (n = 8), or non-myeloablative (n = 2). Donors were HLA-matched related (n = 4), HLA-matched unrelated (n = 16), HLA-haploidentical (n = 2), or HLA-mismatched unrelated (n = 8). After a median follow-up of 2 years (range: 0.5-16 years), 2-year OS was 97%, and 2-year GvHD-free relapse-free survival was 73%. The hematological and immunological phenotypes resolved, and there were no new vascular events. Plasma ADA2 enzyme activity normalized in 16/17 patients tested. Six patients required more than one HCT. CONCLUSION: HCT was an effective treatment for DADA2, successfully reversing the refractory cytopenia, as well as the vasculopathy and immunodeficiency. CLINICAL IMPLICATIONS: HCT is a definitive cure for DADA2 with > 95% survival

Hematopoietic Cell Transplantation Cures Adenosine Deaminase 2 Deficiency : Report on 30 Patients

Correction; Early Access: ' DOI: 10.1007/s10875-022-01280-y Early Access: APR 2022Purpose Deficiency of adenosine deaminase 2 (DADA2) is an inherited inborn error of immunity, characterized by autoinflammation (recurrent fever), vasculopathy (livedo racemosa, polyarteritis nodosa, lacunar ischemic strokes, and intracranial hemorrhages), immunodeficiency, lymphoproliferation, immune cytopenias, and bone marrow failure (BMF). Tumor necrosis factor (TNF-alpha) blockade is the treatment of choice for the vasculopathy, but often fails to reverse refractory cytopenia. We aimed to study the outcome of hematopoietic cell transplantation (HCT) in patients with DADA2. Methods We conducted a retrospective study on the outcome of HCT in patients with DADA2. The primary outcome was overall survival (OS). Results Thirty DADA2 patients from 12 countries received a total of 38 HCTs. The indications for HCT were BMF, immune cytopenia, malignancy, or immunodeficiency. Median age at HCT was 9 years (range: 2-28 years). The conditioning regimens for the final transplants were myeloablative (n = 20), reduced intensity (n = 8), or non-myeloablative (n = 2). Donors were HLA-matched related (n = 4), HLA-matched unrelated (n = 16), HLA-haploidentical (n = 2), or HLA-mismatched unrelated (n = 8). After a median follow-up of 2 years (range: 0.5-16 years), 2-year OS was 97%, and 2-year GvHD-free relapse-free survival was 73%. The hematological and immunological phenotypes resolved, and there were no new vascular events. Plasma ADA2 enzyme activity normalized in 16/17 patients tested. Six patients required more than one HCT. Conclusion HCT was an effective treatment for DADA2, successfully reversing the refractory cytopenia, as well as the vasculopathy and immunodeficiency. Clinical Implications HCT is a definitive cure for DADA2 with > 95% survival.Peer reviewe

Correction to: Hematopoietic cell transplantation cures adenosine deaminase 2 deficiency: report on 30 patients

Correction to: Journal of Clinical Immunology (2021) 41:1633–164