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Biomedical subjects

R Albin

Publications and source records attributed to R Albin.

At least 19 recordsLinked to original sources
PubMed2005

TEACH-M: A pilot study evaluating an instructional sequence for persons with impaired memory and executive functions.

PRIMARY OBJECTIVE: The purpose of this pilot study was to evaluate an instructional package that facilitates learning and retention of multi-step procedures for persons with severe memory and executive function impairments resulting from traumatic brain injury. RESEARCH DESIGN: The study used a multiple baseline across participants design. METHODS AND PROCEDURES: Four participants, two males and two females, ranging in age from 36-58 years, were taught a 7-step e-mail task. The instructional package (TEACH-M) was the experimental intervention and the number of correct e-mail steps learned was the dependent variable. MAIN OUTCOMES AND RESULTS: Treatment effects were replicated across the four participants and maintained at 30 days post-treatment. Generalization and social validity data further supported the treatment programme. CONCLUSIONS: The results suggest that individuals with severe cognitive impairments are capable of learning new skills. Directions for future research include application of the instructional package to other multi-step procedures.

Adult↗
PubMed2000

A mutation in a case of early onset narcolepsy and a generalized absence of hypocretin peptides in human narcoleptic brains.

We explored the role of hypocretins in human narcolepsy through histopathology of six narcolepsy brains and mutation screening of Hcrt, Hcrtr1 and Hcrtr2 in 74 patients of various human leukocyte antigen and family history status. One Hcrt mutation, impairing peptide trafficking and processing, was found in a single case with early onset narcolepsy. In situ hybridization of the perifornical area and peptide radioimmunoassays indicated global loss of hypocretins, without gliosis or signs of inflammation in all human cases examined. Although hypocretin loci do not contribute significantly to genetic predisposition, most cases of human narcolepsy are associated with a deficient hypocretin system.

Adult↗
PubMed1999

Widespread alterations of alpha-synuclein in multiple system atrophy.

Glial cytoplasmic inclusions (GCI) are the hallmark of multiple system atrophy (MSA), a rare movement disorder frequently associated with autonomic dysfunction. In this study of 21 cases of MSA, GCI were consistently immunoreactive for alpha-synuclein and double-immunostained for ubiquitin and oligodendroglial markers, but not glial fibrillary acidic protein. No statistically significant difference was found in the density of GCI in various brain regions in the two forms of MSA, striatonigral degeneration (SND) and olivopontocerebellar atrophy (OPCA). Postmortem brain samples from 9 cases of MSA were fractionated according to solubility in buffer, Triton-X 100, sodium dodecyl sulfate (SDS), and formic acid, and alpha-synuclein immunoreactivity was measured in Western blots. Total alpha-synuclein immunoreactivity was increased in MSA compared to controls, with no statistically significant difference between SND and OPCA. Most of the increase was due to alpha-synuclein in SDS fractions. In controls this fraction had little or no immunoreactivity. In 7 cases and 4 controls correlations were investigated between quantitative neuropathology and biochemical properties of alpha-synuclein. Surprisingly, the amount of SDS-soluble alpha-synuclein correlated poorly with the number of GCI in adjacent sections. Furthermore, areas with few or no GCI unexpectedly had abundant SDS-soluble alpha-synuclein. These findings provide evidence that modifications of alpha-synuclein in MSA may be more widespread than obvious histopathology. Moreover, these alterations may constitute a biochemical signature for the synucleinopathies.

Aged↗
PubMed1997

The neuronal NOS inhibitor L-MIN, but not 7-NINA, reduces neurotoxic effects of chronic intrastriatal administration of quinolinic acid.

Rat striata were exposed to 15 mM quinolinic acid (QUIN), or QUIN plus the nitric oxide synthase inhibitors S-methyl-L-thiocitrulline dihydrochloride (L-MIN) or 7-nitroindazole monosodium salt (7-NINA) for 21 days. Co-administration of 100 microM or 1 mM L-MIN with QUIN significantly reduced lesion volume compared to QUIN alone. Co-administration of 1 microM or 10 microM L-MIN with QUIN had no significant effect. There was no significant effect of 7-NINA co-administered with QUIN compared to QUIN alone. L-MIN reduction of lesion volume supports the contention that neuronal nitric oxide synthase is a mediator of excitotoxic injury.

Animals↗
PubMed1997

SCH 43478 and analogs: in vitro activity and in vivo efficacy of novel agents for herpesvirus type 2.

SCH 43478 and analogs are a class of non-nucleoside antiviral agents that have potent and selective activity against herpes simplex virus type 2 (HSV-2). The IC50 for these compounds in plaque reduction analysis using Vero cells ranges from 0.8 to 2.0 microg/ml. All compounds have a LC50 > 100 microg/ml in cytotoxicity analysis. Mechanism of action studies suggest that these molecules have an effect on the transactivation of viral immediate early (alpha) gene expression. Time of addition studies indicate that antiviral activity of these analogs is limited to the initial 2-3 h after infection and is not due to inhibition of viral adsorption or penetration. Analysis of HSV protein expression demonstrates that SCH 49286 inhibits the accumulation of viral immediate early (alpha) gene products. SCH 43478 demonstrates statistically significant efficacy (P < 0.05) in the guinea pig genital model of HSV infection. Following subcutaneous administration in a therapeutic treatment regimen, SCH 43478 (90 mg/kg/day) is efficacious in reducing the number and severity of lesions and the neurological complications of acute HSV infection. Thus, SCH 43478 and analogs are anti-herpesvirus agents with a unique mechanism of action.

Adsorption↗
PubMed1997

Equilibrium versus compartmental analysis for assessment of the vesicular monoamine transporter using (+)-alpha-[11C]dihydrotetrabenazine (DTBZ) and positron emission tomography.

This work compares equilibrium to kinetic analysis of positron emission tomography data for the assessment of vesicular monoamine transporter (VMAT2) binding density using (+)-alpha-[11C]dihydrotetrabenazine ((+)-alpha-[11C]DTBZ). Studies were performed for 80 minutes after intravenous administration of 18 +/- 1 mCi (+)-alpha-[11C]DTBZ on 9 young control subjects, 20 to 45 years of age. A 9-mCi bolus was injected over the first minute of the study, whereas the remaining 9 mCi were infused at a constant rate over the following 79 minutes. Steady-state was reached in both blood and brain by approximately 30 minutes after initiation of the study. Nonlinear least-squares analysis using two- and three-compartment models, weighted integral analysis using a two-compartment configuration, and Logan plot analysis all yielded kinetic estimates of the total tissue distribution volume, DVtot(kin). These results were compared with equilibrium distribution volume estimates, DVtot(eq), calculated from the tissue to metabolite corrected arterial plasma concentration ratio after 30 minutes. Kinetic modeling results from this study were in close agreement with prior bolus-injection (+)-alpha-[11C]DTBZ studies. In the current study, coefficients of variation in DVtot(kin) (19% to 23% across regions) and DVtot(eq) (18% to 22%) were nearly identical. Equilibrium estimates of DVtot were slightly lower than kinetic estimates, averaging 5% +/- 9% lower (P = 0.04, paired t test) in regions of high binding density (caudate and putamen), but only 2% +/- 6% (P = 0.09) in lower binding density regions (cortex, thalamus, cerebellum). DVtot(eq) estimates, however, still correlated highly with DVtot(kin) estimates (r = 0.977-0.989). Steady-state conditions can be achieved in both tissue and blood by 30 minutes, and the tissue-to-blood ratios of (+)-alpha-[11C]DTBZ at equilibrium yield DVtot(eq) measures that are in close agreement with DVtot(kin) estimates. Thus, a simple, easily tolerated protocol using a loading bolus followed by continuous infusion can provide excellent measures of VMAT2 binding.

Adult↗
PubMed1997

SCH 48973: a potent, broad-spectrum, antienterovirus compound.

SCH 48973 is a novel molecule with potent, selective, antienterovirus activity. In assays of the cytopathic effect against five picornaviruses, SCH 48973 had antiviral activity (50% inhibitory concentrations [IC50s]) of 0.02 to 0.11 microg/ml, with no detectable cytotoxicity at 50 microg/ml. SCH 48973 inhibited 80% of 154 recent human enterovirus isolates at an IC50 of 0.9 microg/ml. The antiviral activity of SCH 48973 is derived from its specific interaction with viral capsid, as confirmed by competition binding studies. The affinity constant (Ki) for SCH 48973 binding to poliovirus was 8.85 x 10(-8) M. In kinetic studies, a maximum of approximately 44 molecules of SCH 48973 were bound to poliovirus capsid. SCH 48973 demonstrated efficacy in a murine poliovirus model of enterovirus disease. SCH 48973 increased the survival of infected mice when it was administered orally at dosages of 3 to 20 mg/kg of body weight/day. Oral administration of SCH 48973 also reduced viral titers in the brains of infected mice. On the basis of its in vitro and in vivo profiles, SCH 48973 represents a potential candidate for therapeutic intervention against enterovirus infections.

Animals↗
PubMed1996

Paroxysmal dystonic choreoathetosis: tight linkage to chromosome 2q.

Paroxysmal dystonic choreoathetosis (PDC) is characterized by attacks of involuntary movements that last up to several hours and occur at rest both spontaneously and following caffeine or alcohol consumption. We analyzed a Polish-American kindred with autosomal dominant PDC and identified tight linkage between the disorder and microsatellite markers on chromosome 2q (maximum two-point LOD score 4.77; recombination fraction 0). Our results clearly establish the existence of a locus for autosomal dominant PDC on distal chromosome 2q. The fact that three other paroxysmal neurological disorders (periodic ataxia with myokymia and hypo- and hyperkalemic periodic paralysis) are due to mutation in ion-channel genes raises the possibility that PDC is also due to an ion-channel gene mutation. It is noteworthy that a cluster of sodium-channel genes is located on distal chromosome 2q, near the PDC locus. Identifying the PDC locus on chromosome 2q will facilitate discovery of the PDC gene and enable investigators to determine whether PDC is genetically homogeneous and whether other paroxysmal movement disorders are also genetically linked to the PDC locus.

Athetosis↗
PubMed1990

The Epstein-Barr virus BZLF1 gene product activates the human immunodeficiency virus type 1 5' long terminal repeat.

The Epstein-Barr virus immediate-early gene product BZLF1 transactivates the human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR). The BZLF1 gene product caused an 18-fold increase in beta-galactosidase activity from an HIV-1 LTR lacZ expression vector, whereas the HIV-1 transactivator tat caused a 44-fold increase in beta-galactosidase activity. When cells were transfected with both BZLF1 (pEBV-Z) and tat (pTAT3) expression vectors, as well as HIV-1 LTR lacZ plasmid (pLRON), a 214-fold increase in beta-galactosidase activity was observed. This result suggests a synergistic effect of BZLF1 and tat on HIV-1 LTR-directed lacZ gene expression. Analysis of quantitative BZLF1 and tat requirements for maximal HIV-1 LTR activation indicates that BZLF1 does not reduce the amount of tat required for maximal LTR activation, as would be expected if the BZLF1 synergistic effect was due to increased tat gene expression. Thus, coordinate effects of BZLF1 and tat on the HIV-1 LTR or its transcript are probably responsible for synergistic HIV-1 LTR activation.

DNA-Binding Proteins↗
PubMed1988

NMDA receptor losses in putamen from patients with Huntington's disease.

N-Methyl-D-aspartate (NMDA), phencyclidine (PCP), and quisqualate receptor binding were compared to benzodiazepine, gamma-aminobutyric acid (GABA), and muscarinic cholinergic receptor binding in the putamen and cerebral cortex of individuals with Huntington's disease (HD). NMDA receptor binding was reduced by 93 percent in putamen from HD brains compared to binding in normal brains. Quisqualate and PCP receptor binding were reduced by 67 percent, and the binding to other receptors was reduced by 55 percent or less. Binding to these receptors in the cerebral cortex was unchanged in HD brains. The results support the hypothesis that NMDA receptor-mediated neurotoxicity plays a role in the pathophysiology of Huntington's disease.

Cerebral Cortex↗
PubMed1986

The Cpx proteins of Escherichia coli K12. Immunologic detection of the chromosomal cpxA gene product.

Previous studies described lacZ'- and cat'-'cpxA fusion genes whose expression restored to normal all the phenotypic defects associated with cpxA mutations (Albin, R., and Silverman, P. M. (1984) Mol. Gen. Genet. 197, 272-279). Here, we show by DNA nucleotide sequence analysis that the fusion genes encode 241 carboxyl-terminal amino acids of the CpxA polypeptide. Using this information, we constructed a fusion gene containing the same 241 cpxA codons preceded by 1007 codons of beta-galactosidase. The resultant hybrid polypeptide was purified and used to raise an anti-(CpxA polypeptide) antiserum. Using the antiserum, we have identified the chromsomal Escherichia coli K12 cpxA gene product as a 52-kDa polypeptide. The polypeptide showed temperature-sensitive accumulation in a strain carrying both the cpxA2[Ts] and cpxB1 alleles and accumulated to a level higher than normal in cells that carried a high-copy number, cpxA+ plasmid. Immune precipitates of in vitro transcription-translation reactions with cpxA+ plasmids as template also contained a 52-kDa polypeptide, indistinguishable in electrophoretic mobility from the immunoreactive polypeptide synthesized in vivo. Two regions of amino acid sequence at the carboxyl-terminus of the CpxA polypeptide are significantly homologous to corresponding regions of the E. coli K12 EnvZ polypeptide, an inner membrane component that, like the CpxA polypeptide, is required to maintain the protein composition of the cell envelope. The cpxA coding sequence is followed by two repetitive extragenic palindrome sequences in opposite orientation.

Amino Acid Sequence↗
PubMed1984

Physical and genetic structure of the glpK-cpxA interval of the Escherichia coli K-12 chromosome.

Mutations at the cpxA locus of Escherichia coli K-12 affect cellular processes that are not otherwise related. We have now determined the physical and genetic structure of the E. coli chromosome in the region of cpxA (87.5 min). Our results indicate that cpxA is a single gene. Previous studies showed cpxA to be linked to tpiA. We therefore isolated two tpiA+ recombinant plasmids, pRA200 and pRA300, from EcoRI and BamHI digests of F'133, respectively. By genetic complementation or enzyme overproduction, the 9.5 kb EcoRI fragment in pRA200 was shown to include glpK, tpiA and cdh. The 13.6 kb BamHI fragment of pRA300 lacks glpK, but includes tpiA, pfkA and cpxA. Neither fragment complemented a deletion of the rha operon. These data indicate the chromosomal gene order: 87 min-rha-cpxA-pfkA-cdh-tpiA-glpK-88 min. The EcoRI and BamHI fragments overlap in an interval corresponding to about 8.2 kb of DNA. The total region of the E. coli K12 chromosome covered by the two fragments is about 15 kb. A terminal 2 kb EcoRI-BamHI fragment from pRA300 complemented the chromosomal cpxA2[Ts] allele with respect to isoleucine and valine synthesis, RNA bacteriophage sensitivity and surface exclusion in Hfr strains, and envelope protein composition. Complementation occurred when the fragment was subcloned in pBR325 but not when it was subcloned in pBR322, suggesting that the 2 kb fragment lacks expression sequences that are supplied by cat (chloramphenicol acetyltransferase gene) expression sequences of pBR325. The cpxA locus on the E. coli chromosome was established with respect to two chromosomal Tn10 insertions by a combination of genetic and physical analyses. The locus established by those analyses was consistent with the location of the 2 kb EcoRI-BamHI fragment in the physical map of the region. Physical analyses of (rha-pfkA) and (rha-tpiA) deletion strains showed that they lack cpxA and surrounding genes. Since these strains were viable, cpxA is not essential under all growth conditions.

Bacterial Proteins↗
PubMed1984

Identification of the Escherichia coli K-12 cpxA locus as a single gene: construction and analysis of biologically-active cpxA gene fusions.

In the accompanying communication we showed that a 2 kb EcoRI-BamHI restriction fragment from the pfkA-rha interval of the Escherichia coli K-12 chromosome fully complemented a chromosomal cpxA mutation when the fragment was cloned in pBR325. The same fragment cloned in pBR322 lacked any complementing activity. We show here that minicells containing the pBR325 derivative (pRA310) synthesized a 33 kDa polypeptide, designated phi 33, that was not synthesized in minicells containing the pBR322 derivative (pRA311) or either of the parent plasmids. Synthesis of the phi 33 polypeptide did not occur in minicells containing Tn5 insertion alleles of pRA310 that inactivated its cpxA complementing activity. These insertions mapped within the vector cat (chloramphenicol acetyltransferase gene) sequence immediately adjacent to the EcoRI site of pRA310 and within the 700-800 bp of the cloned EcoRI-BamHI fragment immediately adjacent to the EcoRI site. Tn5 insertions located within the fragment but closer to the BamHI terminus affected neither the cpxA complementing activity of pRA310 nor synthesis of the phi 33 polypeptide in minicells. Plasmid pRA311 could be converted to a plasmid with cpxA complementing activity by cloning into its EcoRI site a restriction fragment containing a hybrid trp-lacUV5 promoter, the lacZ ribosome binding site, and the first eight lacZ codons.(ABSTRACT TRUNCATED AT 250 WORDS)

Bacterial Proteins↗
PubMed1982

Digital lipoma of the foot: an extraordinary case.

Lipomas, which generally occur in areas of abundant adipose tissue, are rarely found in the foot. The authors describe the surgical procedure in removing a lipoma that totally involved the fourth digit of the right foot of a patient.

Female↗
PubMed1981

Biochemical changes in the collagen of the palmar fascia in patients with Dupuytren's disease.

The palmar fascial tissues of more than 400 patients with Dupuytren's disease were studied biochemically and compared with normal tissue obtained from more than 100 patients who were undergoing hand surgery for other reasons. No alterations of the molecular structure or the state of macromolecular aggregation of the collagen in Dupuytren's disease were detected by wide or low-angle x-ray diffraction studies or by transmission electron microscopy. Major biochemical changes in the palmar fascia affected by Dupuytren's disease included increased collagen and hexosamine contents and the presence of galactosamine in the most severely involved tissue. Type-III collagen, which is virtually absent from normal adult palmar fascia, was abundant in the tissue of patients with Dupuytren's disease. Post-translational modifications included a very elevated hydroxylysine content, an increase in the total number of reducible cross-links, and the appearance of hydroxylysinohydroxynorleucine (virtually absent from normal palmar fascia) as the major reducible cross-link. Even palmar fascia from patients with Dupuytren's disease that appeared grossly and histologically normal showed the same biochemical changes, albeit to a lesser extent. All of these biochemical changes are similar to those that occur during the active stages of connective-tissue wound repair. This includes the rapid synthesis and turnover of collagen which leads to newly synthesized, immature collagen being more abundant in the involved tissue than in normal tissue. There is no evidence that the gross, macroscopic contracture of the palmar fascia in Dupuytren's disease is due to shortening, plication, or contraction of the collagen fibrils or fibers present in the tissue at the onset of the disease or synthesized during its development. Instead, we propose that the gross contracture (shortening) of the palmar fascia in Dupuytren's disease is due to an active cellular process that progressively draws the distal extremities of the affected tissue closer together at the same time that the original tissue is being replaced. The result of these two processes is simply a shorter, smaller piece of tissue fabric containing collagen molecules, fibrils, and fibers of normal length and organization, but with pretranslational and posttranslational modifications similar to those observed in collagens during the active stages of connective-tissue repair in general.

Adult↗
PubMed1979

Diagnosis and treatment of pansinusitis: report of case.

A case of acute pansinusitis with the complication of orbital cellulitis has been described. The patient initially had pain around the maxillary right first molar. Accurate diagnosis allowed for prompt, vigorous treatment, culminating in surgical intervention. The need for dental and oral surgical practitioners to be thoroughly familiar with all of the manifestations of paranasal sinus disease cannot be overemphasized.

Cellulitis↗