HYSTERICAL APNEA IN THE WORK OF GALEN (CA 129 - 199 AD): GENDER EQUITY IN THE HISTORY OF PSYCHOSOMATIC MEDICINE.

OBJECTIVE: The aim: To presents clinical, epidemiological and pathophysiological aspects of the disease described by Galenos of Pergamon during the 2nd century AD and discusses its implications on contemporary discourse on gender equity and gender - based discrimination. PATIENTS AND METHODS: Materials and methods: The authors searched original medical texts written in Greek language and attributed to Galenos for records related to hysterical apnea. CONCLUSION: Conclusions: Galen attempted to interpret hysterical apnea by combining clinical and epidemiological observations with anatomical and functional lesions. His approach denounced the anatomically unsound notion of the wandering womb and availed the knowledge of his period in a rational manner. Investigating gender - related aspects of contemporary psychosomatic conditions related to fertility and pregnancy can help address gender - based discrimination in modern societies.

Migration and newborn screening: time to build on the European Asylum, Integration and Migration Fund?

PURPOSE: The authors discuss the need for newborn screening in the context of the migration policy of the European Union, and particularly, the European Asylum, Migration and Integration Fund. METHODS: The authors searched scholarly databases (Pubmed, Scopus, Google scholar) and grey literature (LexEuropa, Policy reports) to identify original peer-reviewed research examining the migration to the European Union and the provision of healthcare to infants born to refugees and immigrant mothers. Resources in language different from English, French, German and Greek were not taken into consideration. RESULTS: Every year, a large number of refugees and immigrants from sub-Saharan Africa and Middle East countries travel to and enter in Europe. It has been estimated that two thirds of those seeking asylum are women and children. Many of these children have been born on the way to Europe or in migrant camps. Essential newborns' health screening is not accessible in most cases. Congenital conditions such as hypothyroidism and phenylketonuria may remain untreated, and once these infants are diagnosed, the organic damage could be irreversible. Prolonged necessary hospitalisation might be out of consideration at a time when clinics and hospitals are overstrained with COVID-19 patients. CONCLUSIONS: It is essential to ensure that newborn screening will be performed in a timely and evidence-based manner as well as that the information will be communicated between hospitals and within countries' health networks. In order to achieve these goals interdisciplinary and international technical and logistical collaboration are required.

Gene Therapy for Angelman Syndrome: Contemporary Approaches and Future Endeavors.

BACKGROUND: Angelman Syndrome (AS) is a congenital non inherited neurodevelopmental disorder. The contemporary AS management is symptomatic and it has been accepted that gene therapy may play a key role in the treatment of AS. OBJECTIVE: The purpose of this study is to summarize existing and suggested gene therapy approaches to Angelman syndrome. METHODS: This is a literature review. Pubmed and Scopus databases were researched with keywords (gene therapy, Angelman's syndrome, neurological disorders, neonates). Peer-reviewed studies that were closely related to gene therapies in Angelman syndrome and available in English, Greek, Ukrainian or Indonesian were included. Studies that were published before 2000 were excluded and did not align with the aforementioned criteria. RESULTS: UBE3A serves multiple roles in signaling and degradation procedures. Although the restoration of UBE3A expression rather than targeting known activities of the molecule would be the optimal therapeutic goal, it is not possible so far. Reinstatement of paternal UBE3A appears as an adequate alternative. This can be achieved by administering topoisomerase-I inhibitors or reducing UBE3A antisense transcript (UBE3A-ATS), a molecule which silences paternal UBE3A. CONCLUSION: Understanding UBE3A imprinting unravels the path to an etiologic treatment of AS. Gene therapy models tested on mice appeared less effective than anticipated pointing out that activation of paternal UBE3A cannot counteract the existing CNS defects. On the other hand, targeting abnormal downstream cell signaling pathways has provided promising rescue effects. Perhaps, combined reinstatement of paternal UBE3A expression with abnormal signaling pathways-oriented treatment is expected to provide better therapeutic effects. However, AS gene therapy remains debatable in pharmacoeconomics and ethics context.