Problems in studying of Akkadian expression ubānum ištēt ‘one finger’

The Akkadian expression ubānum ištēt ‘one finger’ is found in the Old Babylonian letters of the 18th century BCE, where it is used as an allegoric description of a close alliance between rulers. In the Assyriological literature, there are two possible explanations of the origin of this expression. According to the first one, the allegory of ‘one finger’ was based on a symbolic gesture performed by the kings while concluding a treaty. This gesture consisted of joining or locking thumbs or index fingers. The second explanation suggested that the expression ‘one finger’ referred to a phenomenon of syndactyly, i.e. an inborn defect of fusing of two or more fingers. The imagination of ancient Mesopotamians could turn such fused fingers into the symbol of alliance. W. L. Moran, whom these explanations belong to, considered the first one to be the clearest. Other scholars also accepted this explanation. Thus, in 2019 D. Charpin compared the Akkadian expression with a scene of concluding alliance between two Asian rulers of the 1st century AD, as described in the “Annals” of Tacitus. According to the Roman historian, the ceremony included binding the right thumbs of the two rulers. However, no direct proofs from written or iconographic sources from the 2nd millennium BCE were found, which support any of these explanations. The present article suggests considering as an iconographic proof of the first explanation the Ugarit stele, RS 7.116. This stele dates back to the 14th century BCE and likely preserves an iconographic source for concluding an alliance. The two rulers are standing in front of each other with a high table placed between them. On this table are sitting two tablets representing a treaty between the two parties. The rulers lean the elbows of one of their hands against the tablets and join (or are about to join) the fingers of those hands at the height of their heads. If this is so, and the Old Babylonian and Ugarit sources refer to the same gesture, the stele from Ugarit provides a sufficient ground for speculations about continuity of symbolic and legal practices in Syria and Mesopotamia in the 2nd millennium BCE.

ROLE OF THE NOTCH1 GENE IN FORMATION OF AORTIC ANEURYSM

Aim. To evaluate the impact of genetics in development of thoracic aneurysm in patients with tricuspid valve (TAV) and bicuspid aortic valve (BAV) based on the analysis and search for mutations in NOTCH1.Material and methods. In the study, 60 patients included with the dilation of thoracic aorta more than 40 mm and 200 patients with no aortic pathology, included in the comparison group. All patients underwent echocardiographic assessment on Vivid 7 (GE, USA) equipment, by standard protocol. For molecular genetics we utilized the strategy of targeted mutation screening, including the analysis of 10 of 34 exones of the gene NOTCH1, performed with the direct sequencing.Results. Patients with BAV were younger than those with no inborn defect. Arterial hypertension was verified only in every second BAV patient. Also, maximal rates of blood pressure were significantly lower in patients with inborn defects (р<0,02). As a result of genetic analysis in the studied group, in 9 patients with inborn defect and 2 patients with TAV there were 10 variants found of aminoacid replacement in 6 among 10 analyzed exones, of those 5 replacements — synonimic, and the mutation S2449R was found first time. Mutations P1227S, E1305K, R1279H and D1267N were found at the site of Notch1 protein binding with DLL4, of those 3 are highly pathogenic, that could influence the protein-protein interactions Notch1 with DLL4 leading to formation on aneurysm.Conclusion. Mutations P1227S D1267, E1305K in the gene NOTCH1, being highly pathogenic, may lead to the changes of protein functioning via Notch signalling disorder, that is more characteristic for BAV patients.

SOME DETAILS ABOUT TIMUR LANG’S LAMENESS AND ORIGIN

Tīmūr ibn Tarağāī was born in 1336 (or 1334) in the village Khoja Ilğar of the district Kesh in Mawarannahr, by the origin he was from turkified Mongolian tribe Barlās. He is known as Timur Lang, Tamerlane, Tamburlaine, Temir Aksak, which means Lame Timur or Lame Iron: according to ibn 'Arabshah, his name was Tīmūr, which in other languages (probably in Turkish or Persian) pronounced as Tamūr or Tamrlank/Tamarlank and ''he is the Iron ibn Tarağāī in Turkish''. The information of ibn ‘Arabshah about the stealing of sheep is repeated in the Russian source, which inform us that after stealing the sheep they caught, beat him and throw him to feed dogs. They also broke his leg and tigh-bone. The source affirms in surprise that Timur reminded alive and as he was a smith, he tempered his leg with iron and after that he was called Temir AksakLame Iron. The compatible information let us to suppose that the fact of injuring in the leg or in the arm was used later to mask his inborn defects and to present under heroic light, as a result of the injurance in the battle. M. Gerasimov noticed also that there was no trace on the leg which would be result of the injurance and it is more probably that it was an inborn defect.

Prenatal diagnostics of aninborndefects

Prenatal diagnosis offers a wide range of tests that can be carried out at various stages of pregnancy in order to conduct early diagnosis of congenital malformations. The purpose of this publication is to discuss the methodology, suitability and availability of prenatal testing. The detection of anatomical abnormalities in utero and postnatal verification of the diagnosis decreases the risk associated with malformation in a significant way. Prenatal detection of the defect requiring the surgical intervention on the first days of the life is particularly important. Intrauterine diagnosing of the defect allows to implement the diagnostic and healing progression at the newborn directly after the birth. Transport in utero is the safest way of transmitting the child to the high- specialistic centre . The consultative team looking after the mother and the newborn with an inborn defect should be composed of specialists from obstetrics, neonatology, pediatrics, anesthesiology, pediatric surgery and genetics. In the case of prenatal suspicion or detection of the defects that are possible to surgically repair, it seems appropriate to incorporate a pediatric surgeon to the therapeutic team in the moment of detection in the prenatal period. According to the Polish Gynecological Association it is recommended for every pregnant woman to have an ultrasound scan of the foetus at least 3 times during pregnancy. Minimally invasive screening is destined to all pregnant women in Poland, irrespective of the age. Invading examinations are proposed in case of the positive screening (presence of genetic sonographic marker or wrong biochemical test results) or for pregnant women with the past medical history and at the age above 35.

Etiology of Autism: Genetic Influences

Infantile autism was first described by Kanner in 1943.1 Based on the observation that symptoms often began shortly after birth and always by two or three years of age, Kanner believed that autism was caused by an unknown, inborn defect. Because this syndrome was so severe and peculiar, it seemed unlikely to be an understandable outcome of a child's life experiences. In the years since Kanner first described this disorder, research findings have supported his initial interpretations. It is now generally accepted that autism has a biologic cause, and considerable research has been carried out with the aim of uncovering its nature. Both hereditary factors and the prenatal and perinatal environment have been considered. This paper will review the role of genetic factors in the cause of autism; the role of the prenatal and perinatal environment is considered in the paper by Nelson.51 Three types of genetic associations have been described: (1) the familial aggregation of autism, per se—autism is more common in the sibs of affected children; (2) the familial aggregation of other disorders in the family members of autistic children—a variety of disorders that are mild, but probably conceptually related, have recently been described in relatives; and (3) autism appears in association with a few particular disorders of known genetic etiology. FAMILIAL AGGREGATION OF AUTISM Population and Family Studies In most case series and a few population-based studies, the prevalence of autism in the siblings of autistic children has been estimated to be about 2% to 3%.2,3 While this number is small, it is 50 to 100 times greater than the expected rate of autism of 4 to 5 per 10 000 in the population.4,5