Onlay cartilage graft of the alar lateral crus for cleft lip nasal deformities

The onlay cartilage grafting technique is described for treatment of unilateral or bilateral cleft lip nasal deformities. The alar cartilage is exposed through rim and intercartilagenous incisions. The cephalic half of the alar cartilage is excised, similar to the technique of traditional tip rhinoplasty. The harvested cartilage is applied to the intact caudal cartilage in layered fashion and secured with absorbable sutures. If necessary, successive layers may be added. These grafts provide a sturdy, yet delicate framework for a more normal appearing alar rim. We have performed this procedure on 16 patients, ages 10 to 41. Follow-up intervals range from 13 to 40 months, with a mean of 19 months. Results have been rated good-to-excellent by patients and surgeons. There has been no recurrence of the deformity. The only complication has been one nasal vestibule synechia.     

Uptake and release for glutamine and glutamate in a crude synaptosomal fraction from rat brain

[14C]Glutamine uptake in a crude synaptosomal (P2) fraction, (representing the sum of [¹⁴C]glutamine accumulated and [¹⁴C]glutamate formed by hydrolysis), is distinct from glutamate uptake. Glutamine uptake is Na⁺-independent and unaffected by the Na⁺–K⁺-ATPase inhibitor ouabain, whereas glutamate uptake is Na⁺-dependent and inhibited by ouabain. The uptake of both glutamine and glutamate is unaffected by the gamma-glutamyltransferase inhibitor, Acivicin. This indicates that glutamine uptake is not mediated by a carrier, as distinct from that of glutamate, and also not linked to gamma-glutamyl-transferase. Na⁺ affects the distribution of glutamine-derived glutamate by increasing the synaptosomal content and reducing that of the medium. When glutamate release from synaptosomes preloaded with [¹⁴C]glutamate is measured by superfusion technique in order to prevent reuptake, Na⁺ has been found to inhibit release in a non-depolarizing medium (Ringer buffer with no Ca²⁺) of the [¹⁴C]glutamate as well as of endogenous glutamate. The specific activity of the [¹⁴C]glutamine-derived glutamate in the incubation medium is much higher than that in the synaptosomes, indicating that there exists a readily releasable pool of newly formed glutamate in addition to another pool. The latter glutamate pool is partially reduced by Na⁺.Special Issue Dedicated to Dr. Abel Lajtha.     

Subcellular localization of DNA-binding protein BA by immunofluorescence and immunoelectron microscopy

Nonhistone protein BA has been shown to decrease in amount in the chromatin of growth- stimulated normal rat liver (Yeoman et al. 1975. Cancer Res. 35:1249-1255) and in mitogen-stimulated normal human lymphocytes (Yeoman et al. 1976. Exp. Cell Res. 100:47- 55.). Subsequently, protein BA was purified and was shown to prefer to bind to double- stranded A-T-rich DNAs (Catino et al. 1978. Biochemistry. 17:983-987.). Immunization of rabbits with highly purified protein BA has resulted in the production of a specific antibody. A specific immunoreactivity for chromosomal protein BA has been demonstrated by immunoelectrophoresis and double antibody immunoprecipitation analysis with rabbit anti-BA immunoglobulin and IgG fractions. Light microscope examination of normal rat liver crysections by the indirect immunofluorescence procedure has demonstrated a cytoplasmic as well as a nuclear localization for protein BA with a pronounced perinucleolar fluorescence. Immunoelectron microscopy employing the peroxidase antiperoxidase method of antigen localization has confirmed the immunofluorescence data and has show a heterochromatin localization for protein BA. The relationship of the localization of protein BA to gene control in quiescent cells or to configurations of heterochromatin as well as the marked reduction in the amounts of protein BA which occur in stimulated growth states remains to be defined.     

Gene-environment interaction effects on the development of immune responses in the 1st year of life

Asthma is a common disease that results from both genetic and environmental risk factors. Children attending day care in the 1st year of life have lower risks for developing asthma, although the mechanism for this "day care" effect is largely unknown. We investigated the interactions between day care exposure in the 1st 6 mo of life and genotypes for 72 polymorphisms at 45 candidate loci and their effects on cytokine response profiles and on the development of atopic phenotypes in the 1st year of life in the Childhood Onset of Asthma (COAST) cohort of children. Six interactions (at four polymorphisms in three loci) with "day care" that had an effect on early-life immune phenotypes were significant at P<.001. The estimated false-discovery rate was 33%, indicating that an estimated four P values correspond to true associations. Moreover, the "day care" effect at some loci was accounted for by the increased number of viral infections among COAST children attending day care, whereas interactions at other loci were independent of the number of viral infections, indicating the presence of additional risk factors associated with day care environment. This study identified significant gene-environment interactions influencing the early patterning of the immune system and the subsequent development of asthma and highlights the importance of considering environmental risk factors in genetic analyses.