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Biomedical subjects

D R Johnson

Publications and source records attributed to D R Johnson.

At least 271 records · Page 15Linked to original sources
PubMed1979

Crinkly-tail, a mild skeletal mutant in the mouse.

Crinkly-tail, cy, is a new recessive mutant with imperfect penetrance, in chromosome 4 of the mouse. The only abnormality is in the shape of the vertebrae for one, more rarely two, lengths of the region C9 to C14. This is expressed briefly in the 11-day-old embryo as a duplicated tail gut. None of the mechanisms operating in most of the 20 known tail mutants in the mouse operates in crinkly-tail. The defect is probably due to misallocation of the tissue derived from the primitive streak.

Animals↗
PubMed1978

Effect of exposure to lead on maturation of intestinal iron absorption of rats.

The influence of lead on iron absorption was investigated at various stages of development in rat pups exposed to lead first through mothers' milk and later in their solid diet. Hematocrit, hemoglobin, iron absorption, and tissue iron concentration were measured on d 14, 20, 23, 29, 35, 42, and 63 after birth. Both hematocrit and hemoglobin in the lead-exposed group were significantly below control levels at all periods earlier than d 42 and 63, respectively. Absorption of iron ([59Fe]-ferrous citrate in 10(-4)M FeSO4) from intestinal loops measured over 1/2 h remained at preweaning levels (10-12% of total activity added to the loop) for at least 1 wk after weaning in the lead-exposed rats, whereas in control animals iron absorption fell to adult levels (3-4%) at weaning. Spleen weight was significantly elevated in lead-exposed rats compared with control rats at all ages beyond d 14. However, spleen iron content (micrograms of Fe per gram of tissue) was not significantly elevated in the lead-exposed group before d 42. The results indicate that exposure to lead does not reduce iron absorption from the intestinal tract; thus alteration of intestinal iron absorption does not contribute to lead-induced anemia. Indeed, lead-exposed rats demonstrated increased iron uptake.

Aging↗
PubMed1978

A new type of chondrodystrophic mutant in the mouse.

Stumpy is a new chondrodystrophic mutant in the mouse. The condition is inherited as a fully penetrant Mendelian recessive, and is not allelic with brachymorphic, achondroplasia, or stubby-three similar, previously described mutants. No chromosomal position has yet been assigned to the gene. Phenotypically, stumpy mice are chondrodystrophic dwarfs with all cartilage-formed bones in the skeleton affected. The condition differs from the usual chondrodystrophy described in mice in that proximal elements in the limbs are affected more than distal ones.

Achondroplasia↗
PubMed1978

The growth of femur and tibia in three genetically distinct chondrodystrophic mutants of the house mouse.

Growth of femora and tibiae has been measured in mice carrying three distinct chondrodystrophic mutants (achondroplasia cn, brachymorphic bm and stumpy stm) aged 6--128 days, and in normal litter-mates. cn and bm resemble each other in growing slowly until the time of weaning, when growth is interrupted, stm grows strongly at first, but stops at around 14 days. The significance of these findings is discussed.

Achondroplasia↗
PubMed1978

The effect of a single injection of papain on growth of the limb bones of the mouse.

The chondrodystrophic mouse mutant stumpy (stm) shortens proximal limb bones more than distal ones and acts late in development (circa 14 days post partum). It was thought that a late disturbance in bone growth might cause more damage to epiphyses of proximal than distal bones. This was investigated using a single injection of papain on days 8, 10 and 12: shortening of proximal and distal bones was demonstrated, but was similar in all three experimental groups.

Achondroplasia↗
PubMed1977

Ultrastructural observations on stumpy (stm), a new chondrodystrophic mutant in the mouse.

Stumpy (stm) is a new chondrodystrophic mutant in the mouse. Light microscopy of cartilage reveals a slightly increased mitotic rate, more chondrocytes than is usual per lacuna and a wide zone of hypertrophy. Electron microscopy shows that many chondrocytes are in close approximation with some tight junctions: in cartilage from 14-day-old mice there is much interdigitation and folding of the cell membranes of adjacent chondrocytes.

Animals↗
PubMed1977

Further studies on skull growth in achondroplasic (cn) mice.

The morphology of the basioccipital, basisphenoid and mandibular bones in achondroplasic (cn/cn) mice was compared with that of normal siblings. The two bones of the cranial base were markedly reduced in length but not in width. The percentage reduction in the basisphenoid was twice that in the basioccipital bone and of the same magnitude as that previously observed in the long bones of the limbs. This difference may arise because the basisphenoid, like the long bones, grows in length from two cartilaginous growth sites while the basioccipital grows from one cartilaginous and one periosteal site. The mandible of the cn/cn mice was also reduced in size, although to a lesser extent than were the cranial bones and without the ensuing disproportion. The scale of the mandibular changes suggests that they are largely attributable to regulatory responses to the shortened cranium. The finding that the condylar cartilage of the cn/cn mice is reduced in thickness indicates, however, that the cn gene may have a direct effect on condylar chondrocytes.

Achondroplasia↗
PubMed1976

Social work services in a high-risk nursery.

Why should a social worker be on the team of a neonatal intensive-care nursery? Helping parents cope with the crises that arise with high-risk births is only one important reason. Ameliorating staff stress is another. Also, by following up the high-risk babies, the social worker has an opportunity to play a preventive role.

Adoption↗
PubMed1976

Application of a new method for detecting streptococcal nicotinamide adenine dinucleotide glycohydrolase to various M types of Streptoccus pyogenes.

The production of extracellular nicotinamide adenine dinucleotide glycohydrolase (NADase) by Streptococcus pyogenes can easily be demonstrated using the fluorescence of nicotinamide adenine dinucleotide in ultraviolet light occurring on addition of strong alkali. The new method described here uses microtiter plates and can be read with the naked eye. It permits the screening of large numbers of strains in a short time and with minimal amounts of reagents. The sensitivity of the new method proved to be good in comparison with the bisulfite spectrophotometric method. Culture supernatants of 177 group A streptococci were tested for NADase production by the microtiter fluorescence method. We could confirm former findings that strains within a certain M type of S. pyogenes are usually either producers or nonproducers of the enzyme. The usefulness of the test for screening of streptococcal NADase production is discussed.

Cell-Free System↗