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At least 631 records · Page 35Linked to original sources
PubMed2006

[Morphometric variations of the rumen ciliate, Ophryoscolex purkynjei Stein, 1858 (Ciliophora: Entodiniomorphida) from cypriot domestic goats].

The species Ophryoscolex purkynjei and its four formae [O. p. f. purkynjei, O. p. f. bifidobicinctus, O. p. f. bicoronatus and O. p. f. tricoronatus] from the Cypriot domestic goats (Capra hircus) have been investigated from the viewpoint of the diagnostic morphometrical characteristics. Moreover, it was demonstrated that there was significant morphometrical variations among the same formae in different host animals. As the result of our investigation, it has been suggested that all of the morphometrical variations determined may originate from the individual physiological differences of the host animals (e.g. the other ciliate fauna, bacterial population, inter-specific antagonism etc.).

Animals↗
PubMed1991

Identification of four novel delta-globin gene mutations in Greek Cypriots using polymerase chain reaction and automated fluorescence-based DNA sequence analysis.

The molecular basis of most beta-thalassemia syndromes has been defined, while the spectrum of mutations causing delta-thalassemia is not well characterized. In an attempt to identify such mutations, the region encompassing the delta-globin gene from three Greek Cypriot families suspected of having delta-thalassemia was amplified by polymerase chain reaction (PCR), and DNA sequence determined using an automated fluorescence-based sequencer. Four novel mutations were identified: a G----T change at codon 27 that results in an alanine to serine change; a C----T change at codon 116 converting arginine to cysteine; a T----C change at codon 141 converting leucine to proline; and an AG----GG change at the consensus 3'-acceptor site in IVS-2. While the latter is clearly a thalassemic mutation, the low hemoglobin A2 in the first three may be due to either decreased production or instability of the altered delta-globin chain. All four mutations may be detected by PCR amplification of genomic DNA followed by restriction enzyme digestion. Two mutations abolish restriction sites while two create new cleavage sites. Screening for molecular defects that cause delta-thalassemia or unstable delta-globin by PCR amplification and restriction enzyme digestion will lead to correct diagnosis of beta/delta-thalassemia compound heterozygotes and improved genetic counseling.

Autoanalysis↗
PubMed1985

Alpha zero-thalassemia due to recombination between the alpha 1-globin gene and an AluI repeat.

A form of alpha zero-thalassemia found in subjects of Mediterranean origin has been analyzed by gene mapping and DNA sequencing. Homozygotes have the hemoglobin Bart's hydrops fetalis syndrome, while compound heterozygotes for this defect and alpha+-thalassemia have hemoglobin H disease. It results from a deletion that removes 20.5 kilobases of DNA from within the alpha-globin gene cluster. Sequence data from the regions adjacent to the breakpoint indicate that the recombination event that caused this deletion occurred between the alpha 1-gene and an unusual AluI sequence located between the embryonic zeta genes.

Chromosome Deletion↗