Modern scientific and practical approaches to the production of substrates from semiconductor compounds А3В5. Review

Modern electronic and optical engineering uses А3В5 single-crystal semiconductor materials (GaAs, GaSb, InAs, InSb, and InP) as substrates for epitaxial growth. These materials are obtained in the form of massive single-crystal ingots. Therefore, technologies for processing of these A3B5 wafers are developed to produce the substrates for epitaxial growth. The miniaturization of modern systems and devices demands the high quality of the substrates surface. One of the main criteria is a low surface roughness (Ra) (of about 0.5 nm). To meet this requirement, it is necessary to elaborate the existing methods of surface treatment. The review analyses the current approaches to the treatment of the surface of semiconductor wafers of А3В5 single-crystal materials. It considers the specifics of wafers machining followed by their polishing. The article also presents an analysis of the polishing methods. It reveals that at the moment the chemical-mechanical polishing of А3В5 wafers is the most commonly used method. The review presents the main parameters of this process and systematizes the existing theoretical approaches. The analysis determined the key tendencies in the development of chemical-mechanical polishing of semiconductor А3В5 wafers aimed at increasing the quality of wafers. The article also analyses the latest studies regarding the methods of chemical polishing as an alternative to chemical-mechanical polishing. The next section focuses on surface passivation methods used upon obtaining wafers with a low roughness. Passivation is performed to reduce the reactivity of the surface and stabilize surface states of wafers. A classification of passivation methods is suggested based on the obtained chemical composition of the surface, when the passivation layers are created using oxidation, sulfidizing, or nitriding. Another classification is based on the method of creating passivating coatings and includes wet chemical methods and physico-chemical method

S-Nitrosylation of Surfactant Protein-D Controls Inflammatory Function

The pulmonary collectins, surfactant proteins A and D (SP-A and SP-D) have been implicated in the regulation of the innate immune system within the lung. In particular, SP-D appears to have both pro- and anti-inflammatory signaling functions. At present, the molecular mechanisms involved in switching between these functions remain unclear. SP-D differs in its quaternary structure from SP-A and the other members of the collectin family, such as C1q, in that it forms large multimers held together by the N-terminal domain, rather than aligning the triple helix domains in the traditional “bunch of flowers” arrangement. There are two cysteine residues within the hydrophobic N terminus of SP-D that are critical for multimer assembly and have been proposed to be involved in stabilizing disulfide bonds. Here we show that these cysteines exist within the reduced state in dodecameric SP-D and form a specific target for S-nitrosylation both in vitro and by endogenous, pulmonary derived nitric oxide (NO) within a rodent acute lung injury model. S-nitrosylation is becoming increasingly recognized as an important post-translational modification with signaling consequences. The formation of S-nitrosothiol (SNO)-SP-D both in vivo and in vitro results in a disruption of SP-D multimers such that trimers become evident. SNO-SP-D but not SP-D, either dodecameric or trimeric, is chemoattractive for macrophages and induces p38 MAPK phosphorylation. The signaling capacity of SNO-SP-D appears to be mediated by binding to calreticulin/CD91. We propose that NO controls the dichotomous nature of this pulmonary collectin and that posttranslational modification by S-nitrosylation causes quaternary structural alterations in SP-D, causing it to switch its inflammatory signaling role. This represents new insight into both the regulation of protein function by S-nitrosylation and NO's role in innate immunity

Dissecting the Shared Genetic Architecture of Suicide Attempt, Psychiatric Disorders, and Known Risk Factors

Background Suicide is a leading cause of death worldwide, and nonfatal suicide attempts, which occur far more frequently, are a major source of disability and social and economic burden. Both have substantial genetic etiology, which is partially shared and partially distinct from that of related psychiatric disorders. Methods We conducted a genome-wide association study (GWAS) of 29,782 suicide attempt (SA) cases and 519,961 controls in the International Suicide Genetics Consortium (ISGC). The GWAS of SA was conditioned on psychiatric disorders using GWAS summary statistics via multitrait-based conditional and joint analysis, to remove genetic effects on SA mediated by psychiatric disorders. We investigated the shared and divergent genetic architectures of SA, psychiatric disorders, and other known risk factors. Results Two loci reached genome-wide significance for SA: the major histocompatibility complex and an intergenic locus on chromosome 7, the latter of which remained associated with SA after conditioning on psychiatric disorders and replicated in an independent cohort from the Million Veteran Program. This locus has been implicated in risk-taking behavior, smoking, and insomnia. SA showed strong genetic correlation with psychiatric disorders, particularly major depression, and also with smoking, pain, risk-taking behavior, sleep disturbances, lower educational attainment, reproductive traits, lower socioeconomic status, and poorer general health. After conditioning on psychiatric disorders, the genetic correlations between SA and psychiatric disorders decreased, whereas those with nonpsychiatric traits remained largely unchanged. Conclusions Our results identify a risk locus that contributes more strongly to SA than other phenotypes and suggest a shared underlying biology between SA and known risk factors that is not mediated by psychiatric disorders.Peer reviewe

EARLY CONGENITAL SYPHILITIC PSEUDOPARALYSIS (PARROT’S DISEASE): A CLINICAL CASE

Background. Congenital syphilis is a severe intrauterine infection which, affecting most of the organs and systems of a child, can lead to his disability. However, it is extremely difficult to suspect congenital syphilis in a child in the absence of information about prior syphilis in his mother. The article presents a case of a monosymptomatic clinical picture of early congenital syphilis.Description of the Clinical Case. At the age of 1 month, the child had hyperemia, isolated edema of the right forearm, and restriction of limb movements. He was examined by a pediatrician who suspected a fracture of the forearm bones. X-ray did not show any fracture. The situation was regarded as an allergic reaction; desensitizing therapy was prescribed during which the range of movements in the right arm slightly increased. At the age of 2 months, there was a decrease in the range of movements in the left arm. On admission, the condition was regarded as moderate one. No fever; no signs of intoxication. Skin and visible mucous membranes were not changed. Cardiopulmonary activity was satisfactory. The abdomen was palpable in all compartments, painless. The liver was enlarged 6 cm, of dense consistency. The spleen was enlarged 5 cm. Bowel and bladder functions were normal. Neurological status: the reaction to examination was adequate, emotional cry. Cranial nerves without pathology. Can see and hear. Restricted range of movements in the arms; passive movements were painful. Muscle tone in the arms was low, in the legs — closer to physiological one. Equal and brisk tendon reflexes from the arms and legs. Large fontanel 1.5[1]1.5 cm, not protruded. X-ray examination of the forearm bones showed a change in the structure of the epiphyses of both forearm bones that was common to syphilitic osteochondritis.Conclusion. The article describes the complexity of diagnosis of early congenital syphilis in a child aged 2 months in the absence of a corresponding anamnesis in his mother. The need to rule out syphilitic infection in infants with motor impairments, born from unexamined mothers, has been emphasized

Segmental Allergen Challenge Alters Multimeric Structure and Function of Surfactant Protein D in Humans

Rationale: Surfactant protein D (SP-D), a 43-kD collectin, is synthesized and secreted by airway epithelia as a dodecamer formed by assembly of four trimeric subunits. We have previously shown that the quaternary structure of SP-D can be altered during inflammatory lung injury through its modification by S-nitrosylation, which in turn alters its functional behavior producing a proinflammatory response in effector cells

Effect of Low-Dose Ionizing Radiation on the Expression of Mitochondria-Related Genes in Human Mesenchymal Stem Cells

The concept of hormesis describes a phenomenon of adaptive response to low-dose ionizing radiation (LDIR). Similarly, the concept of mitohormesis states that the adaptive program in mitochondria is activated in response to minor stress effects. The mechanisms of hormesis effects are not clear, but it is assumed that they can be mediated by reactive oxygen species. Here, we studied effects of LDIR on mitochondria in mesenchymal stem cells. We have found that X-ray radiation at a dose of 10 cGy as well as oxidized fragments of cell-free DNA (cfDNA) at a concentration of 50 ng/mL resulted in an increased expression of a large number of genes regulating the function of the mitochondrial respiratory chain complexes in human mesenchymal stem cells (MSC). Several genes remained upregulated within hours after the exposure. Both X-ray radiation and oxidized cfDNA resulted in upregulation of FIS1 and MFN1 genes, which regulated fusion and fission of mitochondria, within 3–24 h after the exposure. Three hours after the exposure, the number of copies of mitochondrial DNA in cells had increased. These findings support the hypothesis that assumes oxidized cell-free DNA as a mediator of MSC response to low doses of radiation