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Biomedical subjects

M Lampe

Publications and source records attributed to M Lampe.

At least 19 recordsLinked to original sources
PubMed2001

Effect of trapped ions on shielding of a charged spherical object in a plasma.

Collisions have traditionally been neglected in calculating the shielding around a small spherical collector in a plasma, and the plasma flow to the collector. We show analytically that, in dusty plasmas under typical discharge conditions, ion charge-exchange collisions lead to the buildup of negative-energy trapped ions which dominate the shielding cloud in the nonlinear region near a dust grain and substantially increase the ion current to the grain, even when the mean-free path is much greater than the Debye length.

Journal Article↗
PubMed2000

Lack of evidence of mitochondrial dysfunction in the offspring of HIV-infected women. Retrospective review of perinatal exposure to antiretroviral drugs in the Perinatal AIDS Collaborative Transmission Study.

A recent report suggesting mitochondrial dysfunction among eight HIV-exposed but uninfected children exposed perinatally to nucleoside reverse transcriptase inhibitors (NRTIs) prompted a review within the Perinatal AIDS Collaborative Transmission Study (PACTS). A standardized retrospective review was conducted of 118 deaths at < 5 years. Deaths were classified as unrelated to mitochondrial dysfunction (Class 1), unlikely related (Class 2), possibly related (Class 3), or likely related or proven (Class 4). Among 35 deaths recorded in HIV-uninfected or indeterminate children, none were classified in either Class 2, 3, or 4. We also reviewed signs or symptoms consistent with possible mitochondrial dysfunction among 1,954 living uninfected children. Only one child was in Class 3 and two siblings were in Class 2; none had perinatal antiretroviral drug exposure. We found no evidence indicating that uninfected infants exposed to perinatal NRTIs died of mitochondrial disorders or that living exposed children had symptoms of mitochondrial dysfunction.

Acquired Immunodeficiency Syndrome↗
PubMed1999

Fragile X syndrome and an isodicentric X chromosome in a woman with multiple anomalies, developmental delay, and normal pubertal development.

We report on an individual with developmental delays, short stature, skeletal abnormalities, normal pubertal development, expansion of the fragile X triplet repeat, as well as an isodicentric X chromosome. S is a 19-year-old woman who presented for evaluation of developmental delay. Pregnancy was complicated by a threatened miscarriage. She was a healthy child with intellectual impairment noted in infancy. Although she had global delays, speech was noted to be disproportionately delayed with few words until age 3.5 years. Facial appearance was consistent with fragile X syndrome. Age of onset of menses was 11 years with normal breast development. A maternal male second cousin had been identified with fragile X syndrome based on DNA studies. The mother of this child (S's maternal first cousin) and the grandfather (S's maternal uncle) were both intellectually normal but were identified as carrying triplet expansions in the premutation range. S's mother had some school difficulties but was not identified as having global delays. Molecular analysis of S's fragile X alleles noted an expansion of more than 400 CGG repeats in one allele. Routine cytogenetic studies of peripheral blood noted the presence of an isodicentric X in 81of 86 cells scored. Five of 86 cells were noted to be 45,X. Cytogenetic fra(X) studies from peripheral blood showed that the structurally normal chromosome had the fragile site in approximately 16% of the cells. Analysis of maternal fragile X alleles identified an allele with an expansion to approximately 110 repeats. FMRP studies detected the expression of the protein in 24% of cells studied. To our knowledge, this is the first patient reported with an isodicentric X and fragile X syndrome. Whereas her clinical phenotype is suggestive of fragile X syndrome, her skeletal abnormalities may represent the presence of the isodicentric X. Treatment of S with 20 mg/day of Prozac improved her behavior. In the climate of cost con trol, this individual reinforces the recommendation of obtaining chromosomes on individuals with developmental delay even with a family history of fragile X syndrome.

Abnormalities, Multiple↗
PubMed1999

FMRP expression as a potential prognostic indicator in fragile X syndrome.

Absence or deficit of FMR1 protein (FMRP) resulting from methylation of full mutation genes is the fundamental defect in fragile X syndrome. We used FMRP immunocytochemistry and detailed phenotypic assessment to investigate the relationship between degree of FMRP expression and the broad clinical spectrum of impairment in 80 individuals affected with fragile X syndrome. FMRP expression correlated with IQ in mosaic males (P=0.043), males with a partially methylated full mutation (P=0.0005), and females with a full mutation (P=0.046). In the females, FMRP expression also correlated with the number of fragile X physical features (P=0.0003). Even modest deficits in FMRP result in some manifestations of fragile X syndrome. In this initial study of 53 males, FMRP expression testing had a very high positive predictive value (100%, confidence interval of 29-100%) for a nonretarded IQ among males with expression of FMRP in > or = 50% of lymphocytes (3 males), suggesting that FMRP expression may have potential as a prognostic indicator in males with fragile X syndrome.

Adolescent↗
PubMed1999

Electrodermal responses to sensory stimuli in individuals with fragile X syndrome: a preliminary report.

The fragile X mutation and fragile X syndrome are associated with hyperarousal, hyperactivity, aggression, and anxiety. These may be related to strong reactions to auditory, tactile, visual, and olfactory stimuli [Hagerman, 1996b; Hagerman and Cronister, 1996]. However, almost no data exist describing hyperarousal and sensory sensitivity in individuals with the fragile X mutation. This study establishes a reliable laboratory paradigm for examining reactions to sensory stimuli. We found the pattern of electrodermal responses (EDRs) to stimulation in one sensory modality predicted the pattern of EDRs in four other sensory systems. In addition, the EDR pattern of individuals with the fragile X mutation was related to their FMR-protein expression. Finally, EDRs in individuals with fragile X syndrome were significantly different from those of normal controls, demonstrating greater magnitude, more responses per stimulation, responses on a greater proportion of trials, and lower rates of habituation. The findings support the theory that individuals with fragile X syndrome have a physiologically based enhancement of reactions to sensations. Because electrodermal activity indexes sympathetic nervous system activity, the data suggest that the over-arousal to sensation may involve the sympathetic system.

Adolescent↗
PubMed1992

[Patients returning after transplantation].

Numerous reports have dealt with patient survival and prognostic factors after renal replacement therapy. However, few data exist for patients after a failed renal transplant and who start dialysis again. With this purpose, we retrospectively studied 36 patients who returned to dialysis after a mean transplantation time of 42.8 +/- 7.8 months. Actuarial patient survival on dialysis after the failed renal transplant (D2) was 78%, 74%, 69% and 41% at 1, 2, 3 and 5 years after restarting dialysis respectively. In comparison, survival of patients who started dialysis without a previous history of a renal transplant showed rates of 91%, 85%, 79% and 64% at 1, 2, 3 and 5 years respectively. The difference was statistically significant only at one year after beginning dialysis therapy (78% vs. 91%, p < 0.025). There were no differences in plasma urea concentration by the time of starting both first (D1) and second (D2) dialysis treatments (37.4 +/- 1.9 and 38.8 +/- 2.9 mmol/L respectively). Instead, a statistically significant difference was found between corresponding serum creatinine values (1100.1 +/- 47.1 and 856.9 +/- 50.0 mumol/L respectively, p < 0.05). When actuarial survival and serum creatinine values at the start of D2 were analyzed, there was a statistically better survival at 1 year for patients with serum creatinine values under 900 mumol/L, as compared with those above 900 mumol/L (85% vs. 52%, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Cloned gene encoding the delta subunit of Bacillus subtilis RNA polymerase.

Core RNA polymerase and several forms of RNA polymerase holoenzyme from Bacillus subtilis are found in association with a 21,500-kDa polypeptide called delta (delta). We have cloned the structural gene (rpoE) for delta by using a hybridization probe a synthetic oligodeoxynucleotide that was designed on the basis of a partial NH2-terminal amino acid (aa) sequence of purified delta protein. The rpoE gene was found to encode a 173-aa polypeptide of a predicted Mr of 20,400. Genetic and physical mapping experiments placed rpoE at 325 degrees on the B. subtilis chromosome and established the gene order rpoE-ctrA-spo0F. The delta subunit is known to enhance the specificity of transcription in vitro by bacterial and phage SP01-modified forms of polymerase, but replacement of rpoE by an in vitro-constructed deletion-mutated gene was found not to impair viability, sporulation, or the growth of phage SP01.

Amino Acid Sequence↗
PubMed1988

[Thallium single photon emission computed tomography following thrombolysis: missing relation to left ventricular function].

To address the question of whether infarct size after thrombolysis can comparably be estimated by thallium SPECT scintigraphy and contrast cineangiography, 32 patients in whom regional wall motion abnormality had been assessed by means of the "centerline" method, 10 to 21 days after infarction, underwent biphasic thallium SPECT scintigraphy with dipyridamole. There were no statistically significant correlations between left ventricular ejection fraction and the degree of hypokinesia in the infarct area on one hand, and thallium defect size in the early and late scintigram on the other. Hypokinesia was inversely correlated (r = -0.51) with the time interval from symptom onset to reperfusion, but no such correlation was found between thallium defect size and this parameter. In patients in whom reperfusion was achieved within 3 h of symptom onset, hypokinesia was significantly less (-1.11 +/- 0.6 standard deviations (SD] than in patients in whom reperfusion was achieved later (-2.16 +/- 0.8 SD; p less than 0.01). Thallium defect size, however, was not different in these two groups of patients. It is concluded that there is no close correlation between regional wall motion abnormality assessed subacutely after thrombolysis and infarct size determined by SPECT in the chronic state. Thus, impairment of left ventricular function may not be assessed from scintigraphic findings.

Adult↗
PubMed1987

Genetic studies of a secondary RNA polymerase sigma factor in Bacillus subtilis.

sigma B (sigma 37) is a secondary species of RNA polymerase sigma factor found in the gram-positive bacterium Bacillus subtilis. To study the function of sigma B genetically, we sought mutations that block the expression of a gene (ctc) known to be transcribed by sigma B-containing RNA polymerase in vitro. One such mutation, called crl, was found to map in or near the structural gene (sigB) for sigma B. To determine directly whether mutations in sigB would prevent transcription of ctc, we replaced sigB in the B. subtilis chromosome with insertion and deletion mutations that disrupted the sigma B coding sequence. Like crl, these in vitro-constructed mutations blocked expression of ctc, but had little or no effect on viability, sporulation, expression of the sporulation gene spoVG, or production of sporulation-associated alkaline protease. Using fusions of ctc to the reporter genes xylE and lacZ, we also identified mutations that enhanced ctc expression. One such mutation, called socB, was found to be located in an open reading frame immediately downstream of sigB.

Bacillus subtilis↗
PubMed1986

Gene encoding the sigma 37 species of RNA polymerase sigma factor from Bacillus subtilis.

sigma 37 is a minor species of RNA polymerase sigma factor found in the Gram-positive bacterium Bacillus subtilis. sigma 37 governs the transcription in vitro of genes that are turned on at an early stage in spore formation, as well as other genes that are switched on at the end of the exponential phase of growth but that are not under sporulation control. To study the role of sigma 37 in B. subtilis gene expression, we have cloned the gene for this minor species of sigma factor in Escherichia coli by using as a hybridization probe a synthetic oligonucleotide that was designed on the basis of the NH2-terminal amino acid sequence of sigma 37 protein. We determined the nucleotide sequence of the entire sigma 37 gene, which was found to encode a 262-amino acid residue polypeptide of 29.9 kDa. The predicted amino acid sequence of sigma 37 showed significant homology to that of other sigma proteins in a region that has been proposed to be the site of binding of these factors to core RNA polymerase. Genetic mapping experiments placed the gene for sigma 37, herein designated sigB, at 40 degrees on the genetic map of Piggot and Hoch [Piggot, P. & Hoch, J. A. (1985) Microbiol. Rev. 49, 158-179]. An insertion mutation was constructed in sigB and found not to impair growth or sporulation.

Amino Acid Sequence↗
PubMed1981

Retinoid effects on epidermal structure, differentiation, and permeability.

Retinoids profoundly influence epidermal differentiation, but neither the nature of their antikeratinizing activity nor their mechanism of action is known. In this study, we have correlated morphologic and histochemical findings with an assessment of stratum cohesion and water barrier integrity in adult hairless mice treated with either 13-cis-retinoic acid or the aromatic retinoid, RO 10-9359. Both the synthetic retinoids produced dose-dependent alterations in transepidermal water loss, which were about 5 to 10 times greater in RO 10-9359-treated animals. In contrast to essential fatty acid deficiency, where diminished intercellular lamellar lipids may account for defective barrier function, these lipid-rich structures were intact in retinoid-treated tissues. Instead, retinoids produced both epidermal and stratum corneum loosening, manifested both by the ready production of intraepidermal friction blisters and by ease of removal of cornified cells by tape stripping. Dyshesion correlated with loss of desmosomes and intra- and intercellular accumulation of amorphous material in the upper epidermis. Since these deposits lacked the tinctorial properties of mucin, dyshesion could not be ascribed to the development of mucous metaplasia. Finally, dyshesion could not be attributed to either gain or loss of membrane sugars demonstrated with rhodamine-conjugated lectins, since these changed only late in the course of retinoid treatment. We conclude that the antikeratinizing basis for retinoid activity comprises: (1) dose-dependent alterations in transepidermal water loss and (2) epidermal and stratum corneum loosening, which may, in turn, lead to loss of epidermal cohesion and abnormal barrier function. Neither mucous metaplasia nor stratum corneum thinning appear to play a major role.

Animals↗