Biomedical subjects
B Bender
Publications and source records attributed to B Bender.
Segmental staining of the murine nephron by monoclonal antibodies directed against the GP-2 subunit of laminin.
Monoclonal antibodies to GP-2, the 220,000-dalton subunit of laminin, were used in an immunohistologic study to investigate structural variations in basement membranes. Mouse kidney was used because of the wide range of basement membranes represented. Two rat/mouse monoclonal antibodies, designated LAM-I and LAM-II were compared with rabbit polyclonal anti-GP-2 in a light and electron microscopic study that identified nephron segments by morphology, by topography, and by the use of markers specific for individual segments. LAM-I staining is demonstrable on all tubular and glomerular basement membranes but not on those of blood vessels or smooth muscle, differing in this respect from anti-GP-2. LAM-II staining is confined to the basement membranes of the convoluted portion of proximal tubule segments (S1 and S2), not the straight (S3) portion; to the thin limb and the thick ascending limb of Henle's loop, but not distal convoluted tubules or collecting ducts. The heterogeneity of GP-2 localization may be due to differing conformations of the molecule at these sites.
Cognitive development of unselected girls with complete and partial X monosomy.
The cognitive development of nine girls with 45,X and 45,X variant karyotypes, seven 45,X mosaics, and nine 46,XX control subjects (ages 8 to 17 years) followed since birth was evaluated. The nonmosaic group was slightly delayed in walking, had a moderately decreased full-scale and performance IQ, demonstrated a striking deficit in perceptual organization and fine motor execution, but had generally average language skills. Three nonmosaic girls with low intelligence were identified and one subject had above average intelligence. Intelligence was not correlated with the presence of physical stigmata. No obvious developmental differences were found between the three girls with 45,X variant, two with partial Xq deletions and one with a ring X chromosome, and the six girls with 45,X genotype. The 45,X mosaic group did not experience early developmental delays and was not significantly different from control subjects on any IQ score. A large amount of variability between subjects was noted, which could be partially attributed to family characteristics and socioeconomic conditions. Whereas this study corroborates previous findings of specific intellectual deficits in 45,X populations, it emphasizes the need for caution in estimating the cognitive development of any X and partial X monosomic infant.
Synthesis of laminin and entactin by F9 cells induced with retinoic acid and dibutyryl cyclic AMP.
Mouse embryonal carcinoma F9 cells were exposed to retinoic acid and dibutyryl cyclic AMP. The treated cells synthesized and secreted into the culture medium the basal lamina components, laminin (GP-1 and GP-2) and entactin. The time course of secretion of the basal lamina components was examined by electron microscopic and immunochemical procedures. The induction of the cells resulted in major morphological changes and the deposition of both laminin and entactin at the cell surface and cell junctions. Intracellular deposits of laminin could be localized to the endoplasmic reticulum and membrane-bound intracytoplasmic vacuoles. Concomitant with the appearance of laminin and entactin, there was a loss of fibronectin synthesis and a marked decrease in a 190,000-Da sulfated glycoprotein that appeared to be related to entactin. In the induced cells, laminin and entactin were associated in a complex that could be dissociated with low concentrations of sodium dodecyl sulfate. The induction of laminin and entactin seem to be independent. The enhanced synthesis of laminin appeared to be under transcriptional regulation since it was found that induced F9 cells contained translatable mRNA for GP-2 when tested in a rabbit reticulocyte lysate system. The uninduced cells did not contain detectable quantities of translatable GP-2 mRNA.
Sex chromosomal anomalies: prospective studies in children.
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Monoclonal antibodies against the GP-2 subunit of laminin.
Two stable rat X mouse hybridoma lines have been isolated. These hybridoma lines produce IgG antibodies directed against the polypeptide portion of the GP-2 subunit of laminin. Antibodies produced by the hybridomas have been shown to be IgG 2b (lambda) and IgG 2a (kappa), respectively. In competition ELISA assays the monoclonal antibodies exhibited different binding affinities for laminin. Furthermore, the two antibodies were partially additive in their reactivity to laminin. Preliminary results also indicate that the antibodies recognized different antigenic determinants in laminin as determined by their reactivity to basement membranes in human and mouse tissues. The monoclonal antibody designated LAM-I stained a broad spectrum of human and mouse tissues; the other monoclonal antibody LAM-II reacted with mouse, but not human tissues. The results indicate that these monoclonal antibodies could be utilized to explore the organization of laminin in basement membranes of different tissues and species.
Speech and language development in 41 children with sex chromosome anomalies.
Forty-one children with sex chromosome anomalies identified from the chromosome screening of a newborn population were blindly evaluated by a speech-language pathologist, along with a control group of 31 siblings. 47,XXX girls and 47,XXY boys were found to have increased problems in auditory perception, receptive language, and expressive language; the problems of the 47,XXY boys were less severe than those of the 47,XXX group, and reflected specific deficits in their ability to process linguistic information rather than a deficit in comprehension. An increased occurrence of speech production problems among the 45,X girls was associated with the presence of oral/structural malformations that often had no measurable effect on their production of speech sounds. Although the 45,X girls and 47,XYY boys had no significant increase of problems in auditory reception, receptive language, and expressive language, the trend of the data suggested more difficulty than in the control groups. The mosaic children were not different from the control subjects. Some children in all groups were found to have normal speech and language development.
Learning disabilities in children with sex chromosome anomalies.
Studies of clinical populations have suggested that genetic factors may be involved in the etiology of learning disabilities. The present study included 44 children (ages 7-16) with sex chromosome anomalies (SCA) who were identified in a 10-year sex chromosome screening of all newborns in 2 large hospitals and thus represents an unbiased sample of children with a genetic etiology. 17 chromosomally normal siblings are included as controls. All subjects were given IQ and achievement tests, and extensive, repeated school histories were taken from parents and school personnel. Results demonstrate that SCA children are at an increased risk for encountering learning problems and receiving special education intervention in school. Furthermore, the nature of the learning disabilities may be karyotype specific, although the results are not invariant within karytypes. 45,X children demonstrate a visuo-spatial deficit as evidenced by lower-performance IQ scores and an increased incidence of handwriting problems, while 47,XXY children experience a verbal language deficit seen in lower verbal IQs and a tendency toward more reading delays. 47,XXX children demonstrate a more global delay crossing most cognitive skill areas, although retardation is rare. Mosaic children are relatively unaffected by their karyotypic variations and hence serve as a second control group which guards against the effects of a negative self-fulfilling prophecy. It is concluded from this evidence that learning disabilities can have a genetic basis, although the specific biological mechanism that affects cognitive development in this population remains elusive.
Sex chromosomal abnormalities (SCA): a prospective and longitudinal study of newborns identified in an unbiased manner.
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Entactin, a novel basal lamina-associated sulfated glycoprotein.
A sulfated glycoprotein, entactin, of apparent molecular weight 158,000 has been isolated from an extracellular basement membrane-like matrix. This matrix is elaborated in cell culture by a mouse endodermal cell line. Antibodies prepared in rabbits against this sulfated glycoprotein react with mouse and rat basement membranes from a variety of tissues. These antibodies also react in a specific manner with a discrete component of mouse and rat kidney glomeruli. The electrophoretic mobility of this component is identical to that of entactin. The mouse kidney antigen, as shown by immunoelectron microscopic studies, is predominantly localized at the surface of epithelial cells of tubules and glomeruli adjacent to the basement membrane. Some antigen is also present in the basal lamina adjacent to the epithelial cells. Entactin is distinct from the basement membrane-associated protein GP-2, a protein similar to laminin. Entactin differs from GP-2 in electrophoretic mobility, cyanogen bromide peptide fragmentation pattern, immunological cross-reactivity, and incorporation of H235SO4. Entactin is insensitive to treatment with chrondroitinase ABC. It is suggested that this molecule plays a role in the interaction of the extracellular matrix and the cell surface.
Duo therapy: a method of casework treatment of children.
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Self-chosen victims: scapegoating behavior sequential to battering.
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Giant premalignant fibroepithelioma.
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