[Swivel luxácia Chopartovho klbu.]. / Swivel Chopart Dislocation.

The authors report a special type of Chopart dislocation named as swivel dislocation or tarsal rotation. This injury is characterized by dislocation of the talonavicular joint but the calcaneocuboid joint remains intact.The foot creates a typical rotational movement but it does not evert or invert. The axis of rotation is interosseous talo-calcaneal ligament, which remains intact. In the reported case the medial swivel dislocation is present in combination with fracture-dislocation of the ankle joint with diaphyseal fracture of fibula and segmental fracture of tibia in the same extremity in multiple injury patient. The typical characteristic and method of treatment of this rare injury are presented. Key words: Chopart dislocation, multiple injuries, therapy, consequence.

[Treatment of Acromioclavicular Dislocations by Weaver-Dunn's Operation.]. / Liecba akromioklavikulárnej luxácie operáciou podla Weavera a Dunna.

The authors present an account of a group of 52 patients subjected to Weaver-Dunn's operation on account of acromioclavicular dislocation grade III. They started to use this method in 1988. The authors emphasize that it is an elastic fixation of the clavicle without the use of osteosynthetic material. It is a simple operation with a relatively short period of work incapacity. Based on the described group of patients the authors provide evidence that they achieved very good results with Weaver-Dunn's operation. Key words: acromioclavicular dislocation, Weaver-Dunn's operation.

A region of the mouse genome homologous to human chromosome 1q21 affects facial clefting.

We sought to determine whether mouse chromosomal regions homologous to human chromosomal regions implicated in the etiology of facial clefting would be related to the incidence of spontaneous cleft palate (CP) or cleft lip with or without cleft palate [CL(P)], Dilantin-induced CL(P), hydrocortisone-induced CP, and/or 6-aminonicotinamide-induced CP. We found that a region on mouse chromosome 3, homologous to human chromosome 1q21, significantly increased the incidence of sporadic CL(P) when the allele from the A/J inbred strain was present. None of the other chromosomal regions or conditions studied had significant associations with this susceptibility to facial clefting, although there was a suggestion that the B allele of the same region was associated with hydrocortisone-induced CP. Thus, the region on human chromosome 1q21 should be further studied for a role in the etiology of human CL(P).

Antisense inhibition of beta-glucuronidase expression in preimplantation mouse embryos: a comparison of transgenes and oligodeoxynucleotides.

Using as a model the inhibition of beta-glucuronidase expression in preimplantation embryos, we have compared injections of transgenes directing the synthesis of antisense RNA and antisense oligodeoxynucleotides to our previous results with cytoplasmic injections of antisense RNAs. Pronuclear injection of an antisense DNA construct containing 1.4 kb of coding region of beta-glucuronidase fused to the mouse metallothionein I promoter results in transient inhibition of gene expression in preimplantation mouse embryos. Pronuclear injection of a smaller antisense DNA construct, overlapping the start codon, failed to inhibit gene expression. Injection of two 20-mer antisense oligodeoxynucleotides, one complementary to sequences including the initiation codon and the second complementary to exon 7 sequences of the beta-glucuronidase gene, failed to inhibit gene expression. In addition, cultures of embryos in the presence of antisense oligodeoxynucleotides had no effect on gene activity. Using radiolabeled oligomers added to the culture medium, we found poor uptake of oligodeoxynucleotides by embryos.

Ectopic expression of chloramphenicol acetyltransferase (CAT) in the cerebellum in mice transgenic for a carbonic anhydrase II promoter-CAT construct that is without apparent phenotypic effect.

We have developed six transgenic lines of mice with constructs containing presumptive 5' regulatory regions of carbonic anhydrase II (CA II). Four of the lines contained 1,100 bases of the 5' flanking region of the human CA II gene, and two transgenic lines resulted from a construct containing 500 bases of the 5' flanking region of the mouse CA II gene. Tissue-specific expression of the chloramphenicol acetyltransferase (CAT) gene was not obtained in any of the transgenic lines. One of the transgenic lines was found to have high levels of expression of CAT in cerebellum. This expression persisted through multiple generations and was independent of the parental origin of the transgene. On the assumption that the expression was due to the insertion of the transgene in or near a gene expressed normally in cerebellum, homozygous mice were bred for the transgenic insert to see if a mutation might have been induced. Homozygous mice were found and seemed to be normal in all aspects of their phenotype studied. Thus, in this case, neither the insertion of the gene nor the ectopic expression of CAT seemed to be harmful to the animals.

Major effects on teratogen-induced facial clefting in mice determined by a single genetic region.

A major correlation has been found between the incidence of glucocorticoid-induced cleft palate and the chromosome 8 segment identified by N-acetyl transferase in mice. The resistant strain became fully susceptible while the susceptible strain became resistant when this chromosomal region, representing less than 0.7% of the genome, was transferred from one strain to the other by the construction of congenic strains. 6-Aminonicotinamide-induced cleft palate and phenytoin-induced cleft lip with or without cleft palate are also influenced by this genetic region but not as strongly. In both cases the susceptible strain became quite resistant to the teratogen-induced clefting when the N-acetyl transferase region of chromosome 8 was transferred. However, this chromosomal region does not make the resistant strain susceptible to these two teratogens.

Genetics of susceptibility to 6-aminonicotinamide-induced cleft palate in the mouse: studies in congenic and recombinant inbred strains.

In a search for genetic differences in susceptibility to cleft palate, congenic and recombinant inbred strains of mice were treated with 6-aminonicotinamide or control injections. Of six loci tested, only the chromosome segment marked by N-acetyl transferase was found to affect susceptibility to 6-aminonicotinamide-induced cleft palate. This chromosome segment is known to affect glucocorticoid-induced cleft palate and phenytoin-induced cleft lip with or without cleft palate in these strains of mice.

HLA antigens, phytohemagglutinin stimulation, and corticosteroid response.

Although it is clear that the major histocompatibility complex is associated with lymphocyte glucocorticoid sensitivity in mice, there has been less evidence for a similar relationship in man. We have typed 158 individuals for: (1) 13 A locus and 16 B locus antigens, (2) degree of stimulation of their purified lymphocytes by phytohemagglutinin A (PHA), and (3) degree of inhibition of the PHA stimulation by prednisolone and prednisolone-21-hemisuccinate. In contrasts of individuals with a particular antigen (homozygous or heterozygous) with all remaining individuals, HLA-B7 was found to be associated with an enhancing effect on the log stimulation by PHA while other antigens of these series did not have significant associations. In similar contrasts, A10 was associated with a decrease in sensitivity to glucocorticoid inhibition of PHA stimulation as measured by the log I50 of the suppression of PHA stimulation. Other antigens of these series were not found to have significant associations with the glucocorticoid sensitivity of lymphocytes in this assay.

HLA-B18 is associated with decreased levels of isoproterenol-stimulated cAMP in lymphocytes.

One hundred fifty-nine individuals were typed for HLA-A and B antigens and levels of isoproterenol-stimulated, lymphocyte cAMP. No significant age, sex, or caffeine effects on the natural log of the lymphocyte cAMP variable (ln cAMP) were found. A comparison of mean ln cAMP levels between individuals who carried a particular antigen (homozygous or heterozygous) and individuals who did not carry the antigen identified a highly significant decrease in ln cAMP levels associated with the HLA-B18 antigen. We estimated that 18.9% of the variability in ln cAMP was attributable to the HLA-B18 antigen. In addition, 38% of the variability in ln cAMP was attributable to factors that aggregate in families that were independent of the HLA-B18 effect. A weaker association of A10 with lymphocyte cAMP might be due to linkage disequilibrium between A10 and B18.