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Biomedical subjects

A LeBlanc

Publications and source records attributed to A LeBlanc.

At least 55 records · Page 3Linked to original sources
PubMed1995

Terminal differentiation-dependent alteration in the expression of translation elongation factor-1 alpha and its sister gene, S1, in neurons.

Elongation factor-1 alpha (EF-1 alpha) is a highly conserved, abundantly expressed protein that functions in peptide elongation during mRNA translation. Mammalian species contain a second EF-1 alpha gene, S1, whose expression is limited to brain, heart, and skeletal muscle. Such tissue specificity in S1 gene expression led us to hypothesize that this specialized member of the EF-1 alpha family is possibly essential to terminally differentiated, long-lived cells such as neurons, cardiomyocytes, and myocytes. We report here that during development, EF-1 alpha mRNA levels remain unchanged in S1-negative tissues, but sharply decrease in S1-positive tissues. RNase protection as well as tissue distribution analyses of the S1 message suggest that down-regulation of EF-1 alpha expression coincides well with that of S1 up-regulation during postnatal development. Analysis of primary cultures of the rat neonatal cerebral cortex cells has shown that S1 gene expression is indeed restricted to neurons only, whereas nonneuronal cell types such as astrocytes and microglia are S1-negative. EF-1 alpha mRNA on the other hand was detected in all three cell types, namely, neurons, astrocytes, and microglia. This report confirms the terminal differentiation-dependent expression of the S1 gene in neurons of the cerebral cortex.

Animals↗
PubMed1995

Hologic QDR 2000 whole-body scans: a comparison of three combinations of scan modes and analysis software.

This study reports on the short-term in vivo precision and absolute measurements of three combinations of whole-body scan modes and analysis software using a Hologic QDR 2000 dual-energy X-ray densitometer. A group of 21 normal, healthy volunteers (11 male and 10 female) were scanned six times, receiving one pencil-beam and one array whole-body scan on three occasions approximately 1 week apart. The following combinations of scan modes and analysis software were used: pencil-beam scans analyzed with Hologic's standard whole-body software (PB scans); the same pencil-beam analyzed with Hologic's newer "enhanced" software (EPB scans); and array scans analyzed with the enhanced software (EA scans). Precision values (% coefficient of variation, %CV) were calculated for whole-body and regional bone mineral content (BMC), bone mineral density (BMD), fat mass, lean mass, %fat and total mass. In general, there was no significant difference among the three scan types with respect to short-term precision of BMD and only slight differences in the precision of BMC. Precision of BMC and BMD for all three scan types was excellent: < 1% CV for whole-body values, with most regional values in the 1%-2% range. Pencil-beam scans demonstrated significantly better soft tissue precision than did array scans. Precision errors for whole-body lean mass were: 0.9% (PB), 1.1% (EPB) and 1.9% (EA). Precision errors for whole-body fat mass were: 1.7% (PB), 2.4% (EPB) and 5.6% (EA). EPB precision errors were slightly higher than PB precision errors for lean, fat and %fat measurements of all regions except the head, although these differences were significant only for the fat and % fat of the arms and legs. In addition EPB precision values exhibited greater individual variability than PB precision values. Finally, absolute values of bone and soft tissue were compared among the three combinations of scan and analysis modes. BMC, BMD, fat mass, %fat and lean mass were significantly different between PB scans and either of the EPB or EA scans. Differences were as large as 20%-25% for certain regional fat and BMD measurements. Additional work may be needed to examine the relative accuracy of the scan mode/software combinations and to identify reasons for the differences in soft tissue precision with the array whole-body scan mode.

Absorptiometry, Photon↗
PubMed1995

Calcium absorption, endogenous excretion, and endocrine changes during and after long-term bed rest.

Negative calcium balance is a known consequence of bed rest, and is manifested in elevated urine and fecal calcium (Ca). Elevated fecal Ca can result from either decreased absorption, increased endogenous fecal excretion, or both. We measured the Ca absorption and endogenous fecal excretion in eight healthy male volunteers before and during 4 months of bed rest. Dual isotope (n = 6) or single isotope (n = 2) methods in conjunction with Ca balance were used to calculate true and net Ca absorption and endogenous fecal excretion. Stool Ca increased from 797 mg/day (mean intake 991 mg/day) to 911 mg/day during bed rest, whereas urine Ca excretion increased from 174 to 241 mg/day. True Ca absorption decreased from 31 +/- 7% of Ca intake pre-bed rest to 24 +/- 2% during bed rest, (p < 0.05) and returned toward pre-bed rest values within 5-6 weeks following reambulation. Endogenous fecal excretion did not change significantly, and therefore, most of the increased fecal Ca resulted from changes in absorption. However, in one individual, endogenous fecal Ca excretion was the major contributor to Ca loss. Ionized Ca and pyridinium crosslinks increased and 1,25(OH)2 vitamin D decreased during bed rest, similar to the decrease in Ca absorption; parathyroid hormone (PTH), calcitonin, serum albumin, phosphorus, and total serum Ca were unchanged. Although alkaline phosphatase, osteocalcin, and PTH were unchanged during bed rest, they were elevated during reambulation. These changes accompanied by increased Ca absorption and balance and decreased ionized and total serum Ca suggest a rebound in bone formation following immobilization.

Absorption↗
PubMed1995

Increased production of 4 kDa amyloid beta peptide in serum deprived human primary neuron cultures: possible involvement of apoptosis.

The etiology of the amyloid beta peptide in sporadic Alzheimer's disease (AD) is not known. Amyloid beta peptide (A beta), a proteolytic product of the amyloid precursor protein (APP), is deposited in the senile plaques and cerebrovascular tissues of individuals with either sporadic or familial AD (FAD). Increased A beta production from mutant APPs in FAD fosters the hypothesis that overexpression of A beta plays a primary role in the pathogenesis of AD. The absence of APP mutations in sporadic AD which displays identical pathological features than FAD such as synapse and neuronal loss, senile plaques and neurofibrillary tangles, suggests other causes for overexpression and/or deposition of A beta. To investigate the effect of neuronal death on APP metabolism and A beta secretion, human primary neuron cultures were induced to undergo apoptosis by serum deprivation. Serum deprived neurons display shrunken and rounded morphology, contain condensed chromatine and fragmented DNA, which are characteristic of apoptosis. In serum deprived neurons, metabolism of APP through the nonamyloidogenic secretory pathway is decreased to 20% from 40% in control cultures whereas 4kDa A beta is increased three- to fourfold. The results suggest that human neurons undergoing apoptosis generate excess A beta and indicates a possible mechanism for increased A beta in the absence of APP mutations.

Amyloid beta-Peptides↗
PubMed1995

Regional muscle loss after short duration spaceflight.

BACKGROUND: Muscle strength and limb girth measurements during Skylab and Apollo missions suggested that loss of muscle mass may occur as a result of spaceflight. Extended duration spaceflight is important for the economical and practical use of space. The loss of muscle mass during spaceflight is a medical concern for long duration flights to the planets or extended stays aboard space stations. Understanding the extent and temporal relationships of muscle loss is important for the development of effective spaceflight countermeasures. HYPOTHESIS: We hypothesized that significant and measurable changes in muscle volume would occur in Shuttle crewmembers following 8 d of weightlessness. METHODS: MRI was used to obtain the muscle volumes of the calf, thigh and lower back before and after the STS-47 Shuttle mission. RESULTS: Statistical analyses demonstrated that the soleus-gastrocnemius (-6.3%), anterior calf (-3.9%), hamstrings (-8.3%), quadriceps (-6.0%) and intrinsic back (-10.3%) muscles were decreased, p < 0.05, compared to baseline, 24 h after landing. At 2 weeks post recovery, the hamstrings and intrinsic lower back muscles were still below baseline, p < 0.05. CONCLUSIONS: These results demonstrate that even short duration spaceflight can result in significant muscle atrophy.

Adult↗
PubMed1994

A role for extracellular matrix degradation and matrix metalloproteinases in senile dementia?

In brain as in cartilage, the extracellular matrix contains aggregates formed by hyaluronic acid (HA) and proteoglycans. In osteoarthritic cartilage, release of the proteoglycans from the aggregates by cleavage of the HA-binding region results in the accumulation of the HA-binding region and in the fragmentation of the released proteoglycans. Stromelysin, a matrix neutral metalloproteinase, is one of the enzymes responsible for the cleavage of the HA-binding region. We suggest that a similar process also occurs in senile dementia. The brain proteoglycan contains sequences identical to those of aggrecan, which are recognized and cleaved by stromelysin, and is, in fact, susceptible to stromelysin digestion. Monoclonal antibodies reacting with glial HA-binding protein, but not with the parent protein, stained several senile plaques as defined by their reactivity with antibodies to the amyloid-beta protein in double-labeling experiments.

Aged↗
PubMed1994

Evaluation of dermal and respiratory chloroform exposure in humans.

Chloroform is a known contaminant of chlorinated drinking water and of swimming pool water disinfected with chlorine or one of its derivatives. Few data exist regarding the importance of dermal and inhalation exposure routes to the chloroform body burden resulting from domestic and recreational use of chlorinated water. In our experimental study involving 11 male swimmers, we quantified the body burden resulting from exposure to various concentrations of chloroform in water and air of an indoor swimming pool, during a daily 55-min exercise period. From the first to the sixth exercise period, CHCl3 mean concentration in water was increased from 159 micrograms/l to 553 micrograms/l. Corresponding mean air CHCl3 level ranged from 597 ppb to 1630 ppb. To dissociate the dermal exposure route from that of inhalation, swimmers used scuba tanks during an additional exercise period. Chloroform concentrations were measured in alveolar air before and after each exercise period, as well as after 35 min of physical activity. Chloroform levels in water and air were measured every 10 min. We examined the relationship between alveolar air concentration (a measure of body burden) at 35 and 55 min and environmental chloroform concentrations by using multiple regression models. The natural logarithm of alveolar air concentration was strongly correlated with aqueous chloroform concentration both at 35 (p2 < 0.001, r2 = 0.75) and 55 min (p < 0.001, r2 = 0.86). The relationship with air concentrations was also statistically significant (35 min: p < 0.001, r2 = 0.58, 55 min: p < 0.001, r2 = 0.63).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Cutaneous↗
PubMed1994

Effects of retained diaphyseal plates on forearm bone density and grip strength.

Numerous complications have been attributed to elective plate removal following successful treatment of both bone diaphyseal forearm fractures, yet the effects of retained implants are not known. Fourteen patients were reviewed for residual forearm grip strength (FGS) and bone mineral density (BMD) following uneventful union. Patients were analyzed in two groups based upon time from fixation: group I, > 2 years but < or = 5 years, and group II, > 5 years. In group I, mean 2.6 years follow-up (n = 6), mean FGS ratios (patient values/age matched general population means) were 0.65 and 0.77, respectively, for plated and normal limbs (p = 0.08). The mean BMD ratios of plated/normal sides adjacent to the plate were 0.99 (ulna) and 1.02 (radius); these values were not significantly different from more proximal forearm BMD ratios (p = 0.92 ulna; p = 0.44, radius). In group II, mean 8.4 years (n = 8), mean FGS ratios were 0.97 and 1.09, respectively, for plated and normal limbs (p > 0.05). The BMD ratio was 1.04 adjacent to the plate; this was not significantly different from the ratios measured away from the plate (p > 0.4). We conclude that retained forearm plates can be well tolerated and that their routine removal is not indicated based on FGS or BMD.

Adolescent↗
PubMed1992

Fatal familial insomnia, a prion disease with a mutation at codon 178 of the prion protein gene.

BACKGROUND: We previously described two members of a family affected by an apparently genetically determined fatal disease characterized clinically by progressive insomnia, dysautonomia, and motor signs and characterized pathologically by severe atrophy of the anterior ventral and mediodorsal thalamic nuclei. Five other family members who died of this disease, which we termed "fatal familial insomnia," had broader neuropathologic changes suggesting that fatal familial insomnia could be a prion disease. METHODS: We used antibodies to prion protein (PrP) to perform dot and Western blot analyses, with and without proteinase K, on brain tissue obtained at autopsy from two patients with fatal familial insomnia, three patients with sporadic Creutzfeldt-Jakob disease, and six control subjects. The coding region of the PrP gene was amplified and sequenced in the samples from the two patients with fatal familial insomnia. Restriction-enzyme analysis was carried out with amplified PrP DNA from 33 members of the kindred. RESULTS: Protease-resistant PrP was found in both patients with fatal familial insomnia, but the size and number of protease-resistant fragments differed from those in Creutzfeldt-Jakob disease. In the family with fatal familial insomnia, all 4 affected members and 11 of the 29 unaffected members had a point mutation in PrP codon 178 that results in the substitution of asparagine for aspartic acid and elimination of the Tth111 I restriction site. Linkage analysis showed a close relation between the point mutation and the disease (maximal lod score, 3.4 when theta was zero). CONCLUSIONS: Fatal familial insomnia is a prion disease with a mutation in codon 178 of the PrP gene, but the disease phenotype seems to differ from that of previously described kindreds with the same point mutation.

Adolescent↗
PubMed1992

Countermeasures against space flight related bone loss.

This paper reviews human data concerning bone loss and attempted countermeasures during spaceflight and bed rest, a commonly employed technique to simulate the effects of weightlessness on the musculoskeletal system.

Bed Rest↗
PubMed1992

Fatal familial insomnia: a second kindred with mutation of prion protein gene at codon 178.

Fatal familial insomnia (FFI), a condition characterized by inability to sleep, dysautonomia, motor disturbances, and selective thalamic atrophy is a prion disease linked to a GAC----AAC mutation at codon 178 of the prion gene. These data were obtained from one kindred. We now report a second kindred affected by FFI and carrying the same mutation. The finding of the same disease phenotype and genotype in a second family further validates FFI as a distinct disease entity and a phenotype of the GAC----AAC mutation at codon 178 of the prion gene.

Base Sequence↗
PubMed1991

Can the adult skeleton recover lost bone?

The loss of bone mineral with aging and subsequent development of osteoporosis is a common problem in elderly women, and as life expectancy increases, in elderly men as well. Space flight also causes bone loss and could be a limiting factor for long duration missions, such as, a Mars expedition or extended occupation of a space station. Before effective countermeasures can be devised, a thorough knowledge of the extent, location, and rate of bone loss during weightlessness is needed from actual space flight data or ground-based disuse models. In addition, the rate and extent that these losses are reversed after return from space flight are of primary importance. Although the mechanisms are not likely to be the same in aging and space flight, there are common elements. For example, strategies developed to prevent disuse bone loss or to enhance the rate of recovery following space flight might have direct applicability to clinical medicine. For various reasons, little attention has been given to recovery of bone mass following space flight. As a prelude to the design of strategies to enhance recovery of bone, this paper reviews published literature related to bone recovery in the adult. We conclude that recovery can be expected, but the rate and extent will be individual and bone site dependent. The development of strategies to encourage or enhance bone formation following space flight may be as important as implementing countermeasures during flight.

Adult↗
PubMed1990

Bone density in eumenorrheic female college athletes.

Information is limited on the effect of exercise on bone density in young eumenorrheic athletes. We studied 12 Caucasian intercollegiate volleyball players (V), nine basketball players (B), ten swimmers (S), and 13 non-athletes (N) with bone density measurements by photon absorptiometry of their calcaneus and lumbar spine (L2-L4). The effect of athletic status on bone density was analyzed by multivariate analysis of covariance, with height and weight as covariates. The bone densities reported below are mean +/- SE, adjusted for the covariates; units = g.cm-2, P less than 0.005. The swimmers had a significantly lower mean density in the lumbar spine than all other groups; the non-athletes' mean density was also lower than that of volleyball players (V = 1.31 +/- 0.03, B = 1.26 +/- 0.04, N = 1.18 +/- 0.03, S = 1.05 +/- 0.03). The volleyball and basketball players' mean calcaneal densities were greater than those of the swimmers and non-athletes (V = 0.530 +/- 0.017, B = 0.564 +/- 0.023, N = 0.438 +/- 0.018, S = 0.375 +/- 0.019). The higher bone densities for athletes in vertical weight-bearing activities are consistent with some but not all published data. The swimmers' low bone density in the lumbar spine, less than published values for amenorrheic runners, was unexpected.

Absorptiometry, Photon↗
PubMed1990

Real-time quality control: the French Minitel system.

A prototype system designed to provide real-time response to inter-laboratory proficiency testing results has been developed using the French Minitel telecommunication system. This nationwide computer networking system allows for instantaneous reporting and evaluation of results obtained on external quality assessment (EQA) samples. If a certain test is in error and presumably out of control the problem can be remedied immediately with obvious advantages to patient care.

Clinical Laboratory Techniques↗