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A M Khaĭder

Publications and source records attributed to A M Khaĭder.

5 recordsLinked to original sources
PubMed1998

[Ultrasonic methods for determining the volume of amniotic fluid in a complicated pregnancy: improved methods for the prognosis of the perinatal outcome].

Semiquantitative measurement of amniotic fluid volume (AFV) was used to predict the pregnancy outcome. In 229 high risk pregnancies, the AFV was assessed by 4 ultrasonographic methods, including our suggested one--the modified amniotic fluid index (MAFI). Abnormal perinatal outcome was defined as operative delivery sue to fetal distress (OD/FD), meconium passage, low 5 min. Apgar score, umbilical artery pH (< 7.2) and intrauterine growth retardation (IUGR). About 26.2%, 32.8%, 37.6%, 30.6% and 16.6% cases of OD/FD, meconium stained fluid, low 5 min. Apgar score, low pH and IUGR were identified with oligohydramnios compared with the normal fluid group, using MAFI (p < 0.000001). The MAFI showed higher significance than the other ultrasonographic (US) methods. With the relative screening performance the sensitivity of MAFI, amniotic fluid index (AFI), maximum vertical pocket (MVP) and tho-diameter pocket (TDP) depths were 91.9%, 70.2%, 58.9% and 32.8% respectively with OD/FD. Our results suggest that the AFV assessment by MAFI may be superior to the other US techniques and it may used in the testing protocols of antepartum fetal surveillance.

Amniotic Fluid↗
PubMedDate not supplied

[Factors that cause a change in the antigenic structure of of the influenza virus hemagglutinin].

Crossing of norakin-resistant mutant NR1 of A/Waybridge (H7N7) strain of fowl plague virus (FPV) with human influenza virus strains produced recombinants inheriting the hemagglutinin (HA) gene of the NR1 mutant and neuraminidase (NA) genes of human influenza virus strains. The R120 recombinant produced by crossing of NR1 with A/Taiwan/1/86 (H1N1) strain, unlike other recombinants and NR1 mutant, lost the capacity of reacting in H1 test with two monoclonal antibodies (MCA) to HA7: 71/4 and 46/6. The ts mutant A/FPV/Rostok which has ts-mutation in HA-gene also had changes in the antigenic specificity of HA. The RA and RB recombinants produced by crossing R120 with the A/Krasnodar/101/59 strain and inheriting HA-gene from R120 and NA-gene from A/Krasnodar/101/59 strain recovered the initial HA antigenic structure. No changes in the antigenic properties of HA were observed in the recombinants produced by crossing the original A/FPV/Waybridge strain with A/Taiwan/1/86 strain and inheriting HA-gene from the original A/FPV/Waybridge strain and NA-gene from A/Taiwan/1/86 strain. It is concluded that ts mutations in influenza virus HA-gene may be accompanied by changes in the antigenic specificity of this virus HA. The possibilities of manifestation of phenotypic suppression at the level of influenza virus virion membrane proteins and the causes of changes in the HA antigenic structure in this virus recombinants are discussed.

Animals↗
PubMedDate not supplied

[Immunogenicity of attenuated reassortants of influenza A virus /Leningrad/134/47/57 (H2N2) for mice, depending on their genome].

Reassortants of cold-adapted strain A/Leningrad/134/47/57 (H2N2) and virulent strain A/PR/8/34 (H1N1), modeling genomic composition of vaccinal strains, were tried in mouse experiments. Reassortants' genomes included the major part (5, 6, or 7) from cold-adapted strain and 1 to 3 genes of virulent strain. All the tested reassortants did not differ by temperature sensitivity or cold adaptation phenotypes, did not cause the death of mice, but differed by the level of reproduction in murine lungs and by immunogenicity. Strains with genomic formulas 6/2 (HA and NA of a virulent strain) and 5/3 (M) (HA, NA, and M of a virulent strain) were characterized by the highest immunogenicity. Reassortants including, besides HA and NA, PA gene 5/3 (PA) or inheriting only HA gene from strain A/pr/8/34 (H1N1) were hyperattenuated and low immunogenic.

Animals↗
PubMedDate not supplied

[The mechanisms of the antiviral action of the bora-adamantane derivative preparation BG-12].

The effect of one of the derivatives of boraadamantane, preparation BG-12, on reproduction of influenza type A and B viruses was studied. This preparation was shown to inhibit multiplication of a wide range of influenza type A and B virus strains. It is important that BG-12 inhibits in cell culture the replication of a mutant of fowl plague virus A/FPV/Weibridge resistant to remantadine. BG-12 was found to exert a marked viricidal effect, to inhibit the hemolytic activity of both influenza A and influenza B viruses, but not the neuraminidase activity of these viruses. The synthesis of some virus-specific proteins was found to be disturbed in influenza B/Ann Arbor/86-infected cells in the presence of BG-12. A FPVBAR mutant of influenza A/FPV/Weibridge (H7N7) virus resistant to BG-12 was obtained. All the BG-12-resistant reassortants inherited genes 4 and 7 coding for hemagglutinin (HA) and membrane proteins (M) from FPVBAR mutant, respectively, and the remaining genes from BG-12-sensitive A/Krasnodar/101/59 (H2N2) virus. The sequencing of a region of the M gene encoding for the transmembrane protein M2 revealed the substitution of Ala30-Thre in this protein. Multiple attempts at generating a mutant of influenza type B virus resistant to BG-12 failed.

Adamantane↗