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Biomedical subjects

J R Archer

Publications and source records attributed to J R Archer.

At least 19 recordsLinked to original sources
PubMed2001

Multistate outbreak of Salmonella serovar Muenchen infections associated with alfalfa sprouts grown from seeds pretreated with calcium hypochlorite.

During September 1999, a multistate outbreak of Salmonella serovar Muenchen infection associated with eating raw alfalfa sprouts was identified in Wisconsin. Despite use of a calcium hypochlorite sanitizing procedure to pretreat seeds before sprouting, at least 157 outbreak-related illnesses were identified in seven states having sprouters who received alfalfa seed from a specific lot. The continued occurrence of sprout-related outbreaks despite presprouting disinfection supports the concern that no available treatment will eliminate pathogens from seeds before sprouting and reinforces the need for additional safeguards to protect the public. A lack of consumer knowledge regarding exposure to sprouts documented in this investigation suggests that more-targeted outreach to high-risk individuals may be needed to reduce their risk.

Adolescent↗
PubMed2001

Maximum life spans in mice are extended by wild strain alleles.

The genes that control basic aging mechanisms in mammals are unknown. By using two four-way crosses, each including a strain derived from wild, undomesticated stocks, we identified two quantitative trait loci that extend murine life spans by approximately 10%. In one cross, the longest-lived 18% of carriers of the D8Mit171 marker allele from the MOLD/Rk strain, Mus m. molossinus, outlived the longest lived 18% of noncarriers by 129 days (P = 5.4 x 10(-5)); in a second cross, carriers of the D10Mit267 allele from the CAST/Ei strain, Mus m. castaneus, outlived noncarriers by 125 days ( P = 1.6 x 10(-6)). In both crosses, P < 1.0 x 10(-4 )is considered significant. Because these life span increases required that all essential biological systems function longer than normal, these alleles most likely retarded basic aging mechanisms in multiple biological systems simultaneously.

Alleles↗
PubMed2000

Heritability of life span in mice and its implication for direct and indirect selection for longevity.

We found high narrow-sense heritability of life span based on the regression of offspring on average parental (midparent) life spans. In two mouse populations prepared using the 4-way-cross design, mean +/- SE heritabilities were 62 +/- 11% (P < 0.001) and 44 +/- 15% (P < 0.01). To reflect inherited rates of aging, rather than resistance to early disease, data from the first 25% to die were deleted, so that only about 40% of families were used for offspring-midparent regressions. Heritabilities still remained high, 38% and 55%, for the same two populations, respectively. Populations studied in two other experiments did not show nearly as high heritabilities; in one case probably due to environmental stress, and in the other probably because the strains used did not have sufficient additive variance in genes regulating longevity. Significant heritabilities occurred only when a wild derived inbred strain was included in the 4-way cross. The age when a female ceased to reproduce appeared to be related to the life spans of her offspring, but only weakly, not approaching significance for any individual experiment. The age when a female became infertile was related to her life span, but the relationship disappeared when short-lived mice were excluded from the analysis. Our findings indicate that, in sufficiently diverse mouse populations, selection for increased longevity should be possible and that the direct selection for parental life span will be a more efficient strategy than selection for female reproductive life span.

Animals↗
PubMed1999

An increase in sporadic and outbreak-associated Salmonella enteritidis infections in Wisconsin: the role of eggs.

In Wisconsin, reported Salmonella enterica serotype enteritidis (SE) infections during 1997 more than doubled compared with the previous 9 years. A case-control study was conducted to determine risk factors for sporadic infections, and results of outbreak investigations were reviewed. Eating raw eggs (matched odds ratio [MOR]=14.5; 95% confidence interval [CI], 1.7-591.6), eating raw or undercooked eggs (MOR=5.8; 95% CI, 1.3-28.0), eating any eggs (MOR=4.2; 95% CI, 1.2-16.2), and dining at a restaurant (MOR=4.7; 95% CI, 1.4-18.4) were associated with infection in the case-control study. For 3 of the 8 outbreaks, a probable source was identified, in each instance, foods containing eggs. Human infections decreased after eggs were diverted from implicated flocks. This epidemic demonstrates the continuing need for quality assurance on egg farms and enhanced education of consumers and commercial food preparers regarding safe handling of eggs.

Adolescent↗
PubMed1997

Cartilage calcification and limb bud growth in the developing tich mouse embryo.

The tich mutation leads to the abnormal development of bones in mice such that a 'V-shaped' tongue of noncalcified cartilage appears in the central portion of the proximal tibial growth plate. In this study, alcian green staining of cartilage glycosaminoglycans was used to demonstrate the pattern of limb development in embryos of stage-matched tich and normal, co-isogenic, A.TL mice from the earliest stages in skeletogenesis. The growth plates of normal A.TL siblings were symmetrical across the limb rudiment whereas the growth plate in tich siblings show the beginnings of a V-shaped tongue of cartilage reaching towards the diaphysis. This showed first at E16.5. It was apparent that the crown rump distance, tibia, ulna, and the length of calcified cartilage in tich were significantly shorter than A.TL. These results confirmed that calcification was not the primary defect in tich but point to a temporal dysfunction in growth factor expression (possibly bone morphogenetic proteins) that stems from early limb bud formation and translates through later stages in development.

Animals↗
PubMed1996

L-deprenyl treatment in aged mice slightly increases life spans, and greatly reduces fecundity by aged males.

Male and female B6D2F1 (C57BL/6J x DBA/2J)F1 and B6CBAF1 (C57BL/6J x CBA/CaHT6J)F1 mice were injected subcutaneously 3 times a week with L-deprenyl (0.25 mg/kg) starting at mean ages of 26 months and 18.5 months, respectively. Life spans of aging mice were increased 6-9% by the drug. While none of the life span effects were significant for a single genotype and gender, life spans were significantly longer in L-deprenyl-treated animals (p = .011) when all data were combined. L-deprenyl-injected mice consumed about the same amounts of food as controls: L-deprenyl 3.1 g/day, control 3.3 g/day, after 7 months of treatment. There were no significant effects of L-deprenyl on measures of changes with age in the following biological systems: activity, excitement, red blood cell mass, collagen denaturation rate, and wound healing rate. L-deprenyl-treated B6CBAF1 males and females were significantly heavier than controls after 4-6 months of treatment. To measure fecundity, B6CBAF1 males at an average age of 750 days were each caged with two young B6 females; 10 of 17 L-deprenyl-injected males sired an average of 31.3 pups per male, while 14 of 24 controls sired 82.1 pups per male.

Aging↗
PubMed1995

Genetics of age-related hearing loss in mice. II. Strain differences and effects of caloric restriction on cochlear pathology and evoked response thresholds.

The effects of genotype and diet on age-related hearing loss were evaluated using auditory brainstem response (ABR) thresholds and post-mortem cochlear histopathology in 5 inbred mouse strains, CBA/H-T6J (CH), DBA/2J (D2), C57BL/6J (B6), BALB/cByJ (BY) and WB/ReJ (WB), and their 10 F1 hybrid strains. The mice had been maintained since weaning on either a high-energy (HE) control diet or low-energy (LE) calorically restricted diet. ABR thresholds were obtained when the mice were 23 months old; the mice were allowed to age until they died from natural causes prior to obtaining the histological material. The severity of post-mortem cochlear pathology in mice maintained with the HE diet supports our earlier genetic model which postulated that B6, BY, and WB strains each possessed a different recessive allele causing age-related hearing loss, D2 mice possessed all 3 genes, and CH mice possessed none. The histopathology indicates that the genes act at the cochlear level. Dietary restriction resulted in increased longevity in a number of strains, but age-related changes in cochlear pathology were not ameliorated in any of these; indeed, in some strains long-lived LE mice exhibited severe cochlear degeneration. In strains for which longevity was not extended by caloric restriction, only B6 mice exhibited an ameliorative effect of the LE diet on cochlear pathology. ABRs in 23-month-olds indicated a slowing of age-related hearing loss in LE mice of 3 F1 hybrid strains.

Analysis of Variance↗
PubMed1995

Cell proliferation within the growth plate of the tich mouse.

The pattern of chondrocyte proliferation was studied in the proximal tibial growth plate of tich mice (gene symbol tch), a recessive mouse mutant, which is coisogenic with the A.TL strain. Specimens were qualitatively studied at time points of 2, 3, 4, 6, and 8 weeks of age by bromodeoxyuridine labeling of cell division and routine histology. At 2 weeks, when the lesion appeared as a full-width thickening of the growth plate, a greater proportion of cells appeared positively labeled in the proliferative zone. This concavity in the central portion of the growth plate became progressively more focal between 3 and 4 weeks to give a "tongue" of unresorbed, noncalcified cartilage in the central region of the tich growth plate. BrdUrd labeling indicated that the appearance of the cartilage tongue corresponded with increased cell division in the central region of the growth plate. At the same time, a "second" zone of cell division formed, within the zone of hypertrophy, such that labeled cells appeared to be set among chondrocytes with hypertrophic morphology. At stages after 4 weeks of age the focal feature disappeared as the growth plate returned to more normal morphology by maturity. It seems that this unique "second" zone of dividing cells may contribute to formation of an elongation of the nonresorbed tongue of cartilage. However, it is not likely to be the primary defect since growth plate changes were apparent at earlier stages.

Animals↗
PubMed1994

Growth plate abnormalities in a new dwarf mouse model: tich.

Growth plate cartilage calcification has been examined in a recently described mouse mutant, tich, which is co-isogenic with the A.TL strain. Long bones were studied from 1-day-old and 1-month-old mice which carried a homozygous recessive gene mutation making them short limbed and dumpy. Specimens were studied by routine histology, scanning electron microscopy and radiography. In 1-day-old tich mice the front of calcified cartilage was recessed behind the advancing periosteum and bone. No similar recess was seen in control mice. At 1 month of age, a number of the long bone growth plates were irregularly thickened, particularly in the central area. This produced a central tongue of non-calcified cartilage (particularly prominent in the proximal tibia) which gave rise to a corresponding pit in the calcified cartilage layer, in macerated specimens. This was accompanied by poor resorption of calcified cartilage. At both ages the presence of the respective defects was radiographically confirmed. At present it is not known whether this is primarily a defect of calcification or resorption but its presence, apparently from a single mutation in a genetically defined mouse strain, makes it a potentially valuable model.

Animals↗
PubMed1993

Chemical reactivity of an HLA-B27 thiol group.

Techniques have been developed to measure the reactivity of free thiols in the HLA class I antigen-binding cleft. HLA-B27, which sequencing predicts has a free cysteine at position 67, reacts rapidly with the positively charged thiol reagent monobromotrimethyl-ammoniobimane bromide (qBBr) to give products which are identifiable by isoelectric focusing. HLA-B38, B39, B64 and B65, all of which have a similar Cys 67, react less strongly. Several other class I molecules, notably HLA-C antigens, are reactive in this system, and it may be capable of recognizing subtypes such as A*0207 which also carry free cysteine. The accessibility of thiol to qBBr depends both on the chemistry of the class I molecule and other factors in the cell. Two human cell lines which are known to carry identical B27 genes but do not present the same peptides, differ considerably in the accessibility of their B27 thiol. Evidence from mouse cells transfected with mutant B27 genes suggests that a unique lysine at position 70 in the wild-type molecule increases reactivity to thiol-reactive metabolites. The failure of B27 to give a complete reaction with qBBr in our model systems suggests that it can exist in more than one chemical form. This may leave the molecule susceptible to oxidation, causing errors in T cell recognition and an exaggerated inflammatory response.

3T3 Cells↗
PubMed1993

Genetics of age-related hearing loss in mice: I. Inbred and F1 hybrid strains.

The auditory-evoked brainstem response (ABR) was used to assess hearing loss in five inbred strains of mice and all ten combinations of F1 hybrids. The inbred strains are CBA/H-T6J (CH), DBA/2J (D2), C57BL/6J (B6), BALB/cByJ (BY) and WB/ReJ (WB). The F1 hybrids are CHD2, CHB6, CHBY, CHWB, D2B6, D2BY, D2WB, B6BY, B6WB, and BYWB. At middle age (12, 16 months), mice were tested with click stimuli. At a relatively old age (23 months, near inbreds' median life span), they were tested with both click and tone-pip stimuli. The CH mice and their four F1 hybrid strains exhibit lower thresholds than the other strains, with the F1 strains being most sensitive (i.e., hybrid vigor). The D2 inbred and the three D2 F1 hybrids (excluding CHD2) exhibit the earliest and most severe hearing losses. The B6, BY and WB inbred strains exhibit severe hearing losses between 16 and 23 months of age; however, the B6BY, B6WB and BYWB F1 hybrids have significantly lower thresholds than their parental strains (genetic complementation). These data support a genetic model for recessive alleles at three different loci which contribute to age-related hearing loss. The CH mice have none of the recessive alleles, and the D2 mice are homozygous recessive for all three; the B6, BY and WB inbred strains are homozygous recessive respectively for one of the three loci.

Acoustic Stimulation↗
PubMed1992

Immune complexes in ankylosing spondylitis.

Immune complexes have been reported in ankylosing spondylitis (AS) and may implicate infectious agents. Serum samples from 49 patients with AS were assayed for immune complexes by polyethylene glycol precipitation, followed by radial immunodiffusion and pepsinogen binding immunoassay. Both methods showed increases in IgA containing immune complexes, which correlated with serum IgA and with IgA rheumatoid factor concentrations, but did not show increases in other immune complex components. Increased immune complexes were associated with peripheral joint synovitis, but showed no correlation with other clinical or laboratory indices of disease activity. Immune complexes from nine AS serum samples and one AS synovial fluid were electrophoretically separated then probed with anti-Klebsiella pneumoniae, but AS specific antigens were not identified. This study did not suggest a major role for immune complexes in AS without peripheral disease, nor provide serological evidence for the involvement of klebsiella antigens.

Antigen-Antibody Complex↗