40 mothers and their 12-month-old infants were observed twice at home by 2 observers for 2 hours. After the second visit, the observers described the infant using the Waters Attachment Behavior Q-sort and the mother's interactive behavior with the Maternal Behavior Q-sort developed by the present authors and Ainsworth's rating scales. Maternal sensitivity was unrelated to maternal age, income, or SES, but correlated positively with maternal education. Mothers of more difficult children were less sensitive. A strong relation was found between infant attachment and maternal sensitivity as measured by the Maternal Behavior Q-sort and by the Ainsworth scales. Using the Q-sort procedure, mothers of more secure infants were more frequently characterized as noticing their babies' signals and using these signals to guide their behavior; they also were more knowledgeable about their infant and appeared to enjoy them more than mothers of less secure infants.

40 mothers and their 12-month-old infants were observed twice at home by 2 observers for 2 hours. After the second visit, the observers described the infant using the Waters Attachment Behavior Q-sort and the mother's interactive behavior with the Maternal Behavior Q-sort developed by the present authors and Ainsworth's rating scales. Maternal sensitivity was unrelated to maternal age, income, or SES, but correlated positively with maternal education. Mothers of more difficult children were less sensitive. A strong relation was found between infant attachment and maternal sensitivity as measured by the Maternal Behavior Q-sort and by the Ainsworth scales. Using the Q-sort procedure, mothers of more secure infants were more frequently characterized as noticing their babies' signals and using these signals to guide their behavior; they also were more knowledgeable about their infant and appeared to enjoy them more than mothers of less secure infants.

A lymphoid-specific transcription enhancer element has recently been identified at the far 3' end of the rat immunoglobulin heavy chain (IgH) locus. Sequence analysis presented here reveals that this enhancer is flanked by a 350-bp invert repeat, giving a structure reminiscent of a transposable element. We therefore screened for the equivalent enhancer in the mouse to determine whether its presence was conserved during evolution. A mouse homologue was indeed identified and is located 16 kb downstream of the C alpha 1 exon. It is also flanked by invert repeats and these are not repeated throughout the genome. The mouse and rat enhancers retain high sequence homology. As regard activity, the IgH 3'-enhancer is lymphoid specific. However, this activity was detected in two plasmacytoma lines tested but not in two B cell lymphomas nor in HeLa cells suggesting that the enhancer may only play a stage-specific role during lymphocyte differentiation. As regards function within the IgH locus, we found that inclusion of the mouse IgH 3'-enhancer (in addition to the intron-enhancer) on mu gene expression plasmids effected a small increase in mu mRNA levels in stable plasmacytoma transfectants.

Olfactory reception occurs via the interaction of odorants with the chemosensory cilia of the olfactory receptor cells located in the nasal epithelium. The cDNA clones from mRNA specific to olfactory mucosa were studied. One of these clones, OBPII, encodes a secretory protein with significant homology to odorant-binding protein (OBP), a protein with broad odorant-binding ability, and is expressed in the lateral nasal gland, which is the site of expression of OBP. The OBPII sequence also shows significant homology to the VEG protein, which is thought to be involved in taste transduction. OBPII is a new member of the lipophilic molecule carrier protein family. The second cDNA clone encodes a novel homologue of glutathione peroxidase, an enzyme involved in cellular biotransformation pathways. Its expression appears to be localized to the Bowman's glands, the site of several previously identified olfactory-specific biotransformation enzymes.

The cluster of genes encoding components of the botulinum neurotoxin (BoNT) complex was mapped in proteolytic (group I) Clostridium botulinum strains encoding BoNT types A, B, and F. Two different arrangements of genes were found: type A strain 62A and type B strain NCTC 7273 have similar organizations of genes encoding BoNT, the nontoxic nonhemagglutinin component (NTNH), hemagglutinin components, and P-21; type F strain Langeland has genes encoding BoNT, NTNH, and P-21, and a previously unidentified open reading frame encoding a protein of 416 amino acids. A group of type A strains typified by infant strain Kyoto-F, which is unlike type A strain 62A, lacks genes for hemagglutinin components and exhibits an organization similar to that of type F. Sequencing and pairwise analysis revealed the presence of possible chimeric sequences in some NTNH genes of proteolytic C. botulinum. Discordance in genealogical trees derived from different regions of the NTNH genes was observed which could be symptomatic of recombination and which may indicate that the NTNH gene represents a hot spot for such events within the cluster of genes encoding the BoNT complex. It is also evident that the phylogenetics of the NTNH gene, which is linked to the gene encoding BoNT, does not mirror the evolutionary history of the BoNT, upon which the C. botuZinum species complex is defined and subdivided.