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Biomedical subjects

L Rowe

Publications and source records attributed to L Rowe.

At least 37 records · Page 2Linked to original sources
PubMed1992

A comparison of two methods of breastfeeding management.

This study has demonstrated that, in a small group of 58 mothers, specific advice focused on establishing easier patterns of breastfeeding resulted in more of them continuing to breastfeed their babies for a longer period post-partum, with a less intense feeding pattern and the use of fewer complementary bottles of formula or other liquids, than did those given only the standard advice about breastfeeding. Current advice might be reviewed to continue to encourage demand breastfeeding but to emphasise the establishment of easier patterns of breastfeeding that optimise the mother-infant interaction.

Adult↗
PubMed1990

The murine situs inversus viscerum (iv) gene responsible for visceral asymmetry is linked tightly to the Igh-C cluster on chromosome 12.

The iv gene controls left-right determination during murine organogenesis. To map this gene, we analyzed backcross progeny produced by mating (C57BL/6J X MEV/Ty)F1-iv/+heterozygotes to C57BL/6J-iv homozygotes. Hybridization of a murine ecotropic virus probe and several homeotic box gene probes coupled with analysis of dominant visible markers enabled us to exclude the iv locus from much of the mouse genome. Spurred by a recent report that mapped the iv gene to mouse chromosome 12 which was not excluded by our previous work, we used the polymerase chain reaction on our larger cohort to determine that the iv gene is indeed linked tightly to the Igh-C locus on this chromosome: we observed 0/156 recombinants between the iv and Igh-C loci. Combining data from the two studies demonstrates that the murine iv gene is close (1/201 recombinants) to the Igh-C cluster on chromosome 12.

Animals↗
PubMed1989

A mouse linkage testing stock possessing multiple copies of the endogenous ecotropic murine leukemia virus genome.

A new linkage testing stock of the laboratory mouse has been constructed. The stock, designated MEV (multiple ecotropic provirus), was developed by inbreeding and selection beginning with the cross of strains C58/J and AKXD-14. Eleven different murine leukemia virus (MuLV) proviruses have been fixed in the MEV/1Ty strain. Nine of these can be uniquely identified by Southern blotting of PvuII-digested DNA and probing with a cloned fragment of the ecotropic viral genome. Two proviruses had been mapped previously to chromosome 7, while single proviruses had been mapped to chromosomes 2, 9, and 11. The mapping of six additional proviruses, derived from C58/J, to chromosomes 1, 3, 5, 10, 18, and 19 is described. Another C58/J provirus was mapped to chromosome 8 and proved to be identical to the previously mapped C58v-1 virus inducibility gene of strain C58/Lw. Three dominant visible markers, hammer-toe (Hm), steel (Sl), and caracul-J (CaJ), located on chromosomes 5, 10, and 15, respectively, have been introduced onto the MEV genetic background by repeated backcrosses to provide additional linkage markers. It is estimated that approximately 50% of the genome can be screened by scoring 50 fully informative gametes from a linkage cross of the MEV-Hm, -Sl, -CaJ stock for the combination of viral and visible markers. A strategy for efficiently mapping new recessive visible mutations by pooling tissues for DNA extraction from mutant homozygotes among F2 progeny is described. Ways of further improving the MEV stock are discussed. The location of the Myb proto-oncogene is defined relative to Sl and one of the C58/J proviruses on chromosome 10.

Animals↗
PubMed1987

Lupus profundus in children: treatment with hydroxychloroquine.

Discoid lupus erythematosus and lupus profundus, rare in children, are described in two young girls, one with onset at 3 1/2 years of age, the other at 8 years of age. Unusual nodules of the face that ultimately healed with atrophy and hyperpigmentation showed histologic and immunofluorescent confirmation of lupus erythematosus. These patients, the second and third in the English literature to be treated for childhood lupus profundus with antimalarials, responded successfully to hydroxychloroquine. No systemic involvement was found.

Child↗
PubMed1987

The congenital goiter mutation is linked to the thyroglobulin gene in the mouse.

Rat thyroglobulin (TG) cDNA clones were used to identify DNA restriction fragment variants among inbred mouse strains. One of these variants was shown to be closely linked to the recessive mutation congenital goiter (cog), which had previously been mapped to mouse chromosome 15. These results indicate that the structural gene for thyroglobulin is on chromosome 15 and suggest that a mutation at the site of the TG gene is the basis of the cog defect. No differences were observed between cog/cog and +/+ DNA in Southern blots using TG cDNA probes corresponding to 88% of the coding sequences, suggesting that the cog mutation is not due to a large deletion of this portion of the gene. Neither was there any obvious qualitative or quantitative difference between mutant and normal TG mRNA as judged by blot hybridization of electrophoretically fractionated thyroid RNAs. The thyroglobulin gene locus (Tgn) was mapped near the glutamic-pyruvic transaminase isoenzyme locus Gpt-1. The Tgn locus is syntenic with the c-myc protooncogene locus (Myc) in the mouse as in the rat and man.

Animals↗
PubMed1987

Anterolisthesis in the cervical spine--spondylolysis.

Two cases of cervical spondylolisthesis are reported, and the relevant English language literature is reviewed. Analysis of data derived from all of the cases reported revealed no statistically significant etiological or prognostic factors. The roentgenological evaluation, including associated anomalous findings, is presented. Etiological and clinical aspects of cervical spondylolisthesis are discussed. It is concluded that cervical spondylolysis is a relatively rare congenital defect. The role of manipulative therapy in the treatment of associated symptoms is discussed.

Adult↗
PubMed1985

Linkage of a 7S RNA sequence and kappa light chain genes in the mouse.

A mouse 7S RNA cDNA plasmid clone was employed to identify and map DNA restriction fragment variants using recombinant inbred (RI) and congenic mouse strains. More than a dozen such restriction variants were identified and mapped to different regions of the mouse genome. One such variant, designated Rn7s-6, showed close linkage to the Ly-2,3-Igk-V (T lymphocyte antigens 2 and 3, kappa immunoglobulin variable region) cluster of markers on chromosome 6. No recombinants were detected among three of these markers in 59 RI strains. On the basis of these data, the Rn7s-6 sequence may be placed within 1.3 centimorgans of Ly-3 and one of the Igk-V-region markers, Igk-Ef1. Two mouse stocks with previously identified crossovers within the Ly-2,3-Igk-V region were used to sublocalize Rn7s-6. The results are consistent with the gene order (Ly-2, Ly-3)-(Rn7s-6, Igk-Ef1)-Igk-Ef2. Several mouse plasmacytomas, known to have various parts of the kappa chain complex deleted, retain the Rn7s-6 sequence. The Rn7s-6 variant is a plus/minus variant; no sequence allelic to Rn7s-6 is found in inbred strains that share the Ly-3a-Igk-Ef1a haplotype.

Animals↗
PubMed1985

African "eosinophilic bodies" in vivo in two American men with Kaposi's sarcoma and AIDS.

Pink-stained (hematoxylin and eosin), variably sized, round-shaped, intracellular and extracellular "eosinophilic bodies," commonly observed in African cases of Kaposi's sarcoma (KS), were discovered in cutaneous KS tumors of two American men with AIDS (the acquired immune deficiency syndrome). These "bodies" were also identified in Gram-, Giemsa-, and Fite-stained (acid-fast) sections. The exact nature of eosinophilic bodies is unknown, but they are thought to be related to Russell bodies. Further study of eosinophilic bodies in KS may shed light on the pathogenesis of these tumors, as they occur in the epidemic of AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Chromosomal assignment of two endogenous ecotropic murine leukemia virus proviruses of the AKR/J mouse strain.

The AKR/J mouse strain is genetically fixed for three different ecotropic murine leukemia virus genomes, designated Akv-1, Akv-3, and Akv-4 (Emv-11, Emv-13, and Emv-14). With recombinant inbred strains and crosses with linkage-testing stocks, Akv-3 and Akv-4 were placed on the mouse chromosome map. Akv-3, which encodes a replication-defective provirus, maps near the agouti coat color locus, a, on chromosome 2. Akv-4, which is replication competent, maps near the neurological mutant gene locus trembler, Tr, on chromosome 11. Akv-1 and Akv-2 (Emv-12), an ecotropic provirus carried by AKR/N but not AKR/J, have previously been mapped to chromosome 7 and 16, respectively. Thus, the four Akv proviruses mapped to date are on four different chromosomes. Akv-3 is the second ecotropic murine leukemia virus provirus to be mapped near the agouti locus. The results are discussed in relation to possible nonrandomness of viral integration.

AKR murine leukemia virus↗
PubMed1984

Genes for serum amyloid A proteins map to Chromosome 7 in the mouse.

Several restriction fragment length variants have been detected among inbred strains using a mouse serum amyloid A cDNA clone. Five variants were shown to segregate as a single genetic unit and were mapped to Chromosome 7 between the glucose phosphate isomerase locus (Gpi-1) and the pink eye dilution locus (p) using recombinant inbred and congenic strains. The finding that no major MspI or BclI restriction fragments were shared between digests of DNAs from a Chromosome 7 congenic strain and its inbred partner, indicate that most, and probably all, sequences detected with the probe are clustered on Chromosome 7. Aneuploid mapping was used to show that the serum amyloid A gene complex (Saa) is proximal to the Chromosome 7 breakpoint in T(7;X)1Ct, a translocation in which the middle third of Chromosome 7 is inserted into the X-chromosome. A survey of inbred strains revealed a single common Saa haplotype and eight rare haplotypes. The complex distribution of 14 different variants suggests that recombination may have played a role in haplotype evolution.

Amyloid↗
PubMed1983

Re-emergence of rinderpest as a threat in East Africa since 1979.

Following the success of the JP15 scheme and subsequent annual vaccination campaigns, East Africa was virtually free of rinderpest after the mid 1960s and the disease was considered beaten. However, economic difficulties have recently reduced the expensively maintained vaccine cover and the disease has reappeared throughout much of the region. In 1979 rinderpest was diagnosed in cattle in north eastern Uganda and caused considerable losses until finally brought under control in 1981. No field outbreaks of the disease in cattle have been seen in Kenya but there is serological evidence that the virus has recently infected unvaccinated sheep and goats and wild ungulates in that country. In 1982 rinderpest was confirmed in the laboratory as the cause of death of large numbers of buffaloes in northern Tanzania and implicated as the cause of a rinderpest-like disease of cattle which is reported to be still active in that area. Substantial aid is essential for further control and research if the virus is not again to become endemic in the region.

Africa, Eastern↗
PubMed1983

Hypocholesterolemia and hypocortisolemia in acute and terminal Babesia bovis infections.

Sera from Babesia bovis-infected cross-bred cows and purebred steers were evaluated throughout the course of acute Babesia bovis infection for cholesterol and cortisol concentrations. Cholesterol and cortisol values of surviving cattle became markedly reduced (less than 50% of normal values) during the acute phase of the disease, Days 10-15 postinoculation, and returned to essentially normal values by the end of the 35 day experimental period. The combined control group values were approximately 2.98 mM/l cholesterol and 0.085 mM/l cortisol throughout the experimental period. The results suggest that if normal synthesis of cholesterol by hepatocytes or other tissues is not maintained, then cholesterol-derived compounds such as cortisol may not be produced at levels adequate to protect against the effects of stress and cell damage during the disease process.

Animals↗
PubMed1982

Hypodermitis sclerodermiformis. Successful treatment with ultrasound.

We report herein the successful use of ultrasound therapy in the treatment of hypodermitis sclerodermiformis (HS). It is a skin disease characterized by well-circumscribed, chronic, painful and tender, single or multiple, board-like, indurated, sharply bordered lesions, occurring on the legs of patients with venous insufficiency. Hypodermitis sclerodermiformis is a little-known clinical entity, often undiagnosed or misdiagnosed as phlebitis, cellulitis, or stasis dermatitis. It merits clinical recognition because of the gratifying and unique response it has to treatment with ultrasound therapy.

Adult↗
PubMed1981

Transposition of yeast mating type genes from two translocations of the left arm of chromosome III.

In the yeast Saccharomyces cerevisiae, the HIS4C gene lies on the left arm of chromosome III. We analyzed two chromosomal rearrangements that have HIS4C translocated either to chromosome XII or to a new translocation chromosome. Using the cmt mutation that allows expression of the normally silent copies of mating type genes, we found that both of these translocations also carried HML alpha, more than 30 map units distal to HIS4C which normally lies on chromosome III. In the case of the translocation chromosome (designated T3), we also found an exchange event between HML alpha on the translocation chromosome and HMLa on chromosome III. In diploids containing two T3 chromosomes (one carrying HML alpha and the carrying HMLa), we found that HML was 32 centimorgans from HIS4C, which was 10 centimorgans from an unknown centromere. In homothallic strains carrying HMLa MATa HMRa on chromosome III, switching from MATa to MAT alpha could occur by using the HML alpha on the translocation as the sole donor of alpha information. Transposition from HML alpha on chromosome T3 was about 20 to 40% as efficient as transposition from intact chromosome III. In contrast, transposition from the HML alpha inserted into chromosome XII was reduced about 100-fold. This reduced efficiency did not appear to be caused by an alteration in the sequences immediately surrounding HML alpha in the translocation. The translocated HML alpha sequence was located in the same size (29-kilobase) SalI fragment as was found in chromosome III, and the same EcoRI, HindIII, and BglII restriction sites were also found. Furthermore, HML alpha was still under the control of the CMT gene, which maintains HML as a silent copy of mating type information. These results suggested that the position of the HML alpha sequence plays an important role in the efficiency of mating type switching.

Base Sequence↗